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Immunology 2015
Midterm and final
| Question | Answer |
|---|---|
| Cytokines | regulate intensity, duration, and characteristics of immune response act on target cells by biding to receptors acre proteins by activated cytokines |
| which of the following statements about inflammation is false? | since inflammation is an immune response it will not cause harm to self tissues |
| inflammation? | an important initiating immune response tht enhances delivery of o2 & clotting factors, promotes the infiltration of WBCs to a site of infection, activated mast cells and macrophages secrete signally molecules that contribute 2 initiation of a response |
| Which of the following is not considered to be a component or characteristic of adaptive immunity? | first response |
| Gene rearrangement events | occur in developing T cells and B cells, are required for assembly of antibodies and T cell receptors, and generate diversity in antibodies and TCRs |
| Which of the following statements about neutrophils is false? | they process and present antigens to T cells |
| What about neutrophils is true? | they are the most abundant leukocyte, they have multi lobed nucleus, they are phagocytes, and they are a major component of pus |
| numerous vaccination procedures require multiple booster shots because? | repeat exposure to an antigen builds up a larger pool of antigen specific memory cells |
| what about CD8T is false? | CD8 binds to the peptide binding domain of the MHC and thus contributes to antigen specificity of CTLs |
| What of the following statements regarding CD8 T cells is correct? | CD8 is referred to as the CD8T co-receptor, activated CD8t cells (CTls) kill pathogen infected cells by inducing apoptosis, and are MHC class-1 restricted |
| Which of the following is not considered to be a component or characteristic of innate immnuity? | antigen specific activation and memory |
| which of the following statements is true? | opportunistic pathogens cause disease in individuals with weak or impaired immune systems |
| What is the alternative pathway? | it binds to the pathogen, covers it in cytokines, and secretes cytokines to recruit other immune cells to fight the infection |
| What is the lecthin mannose pathway? | it recognizes different complexes on the surface of the molecules and thereby binds to them and covers it in protein (opsonizes it) to make it easier to phagocytize |
| what is the classic pathway? | it finds a foreign cell and causes it to be osponized and to have pores in the cell membrane causing it to lyse |
| what is tolerance and what is its significance? | it is about elimination and inactivation of lymphocytes that will attack our own cells |
| What are three fundamental differences between innate and adaptive immunity? | 1 - innate immunity is fast acting, adaptive immunity =slow 1st time 2 - adaptive immunity = memory while innate doesnt keep memory 3 - innate immunity = genetic/generational, adaptive comes through the exposure of the individual |
| What are the primary lymphoid organs? | bone marrow and thymus |
| what are the secondary lymphoid organs? | lymph nodes, spleen, preyers patches, |
| immunoglobulin gene rearrangement during B cell development results u | Assembly of a complete antibody coding sequence that is suitable for expression, and a diversity of antibody specificities |
| the T cell co-receptor CD4 interacts with_________bound to the surface of ___________, | MHC class II; APCs |
| which of the following is not considered an antibody effector function? | cell-cell communication |
| What are the functions of antibody effectors? | neutralization of toxins, ADCC (antibody-dependent cell-mediated cytotoxicity) and, complement activation |
| Which of the following characteristics is common to both t cell receptors and immunoglobulins? | somatic recombination of V, D, and J segments resulting in tremendous diversity of antigen binding sites |
| What corresponds to an antigen binding site? | the pairing of light and heavy chain V regions |
| what is associated with antigen presentation by MHC class 1? | antigens are derived from proteins in the cytosol of the presenting cell |
| Humanization of monoclonal antibodies is done in order to? | avoid HAMA response and create antibodies suitable for clinical treatment of human diseases |
| what describes the sequence of events involved in processing of peptides that will be presented as an antigen with MHC class II? | endocytosis lysosomal protease activity removal of CLIP from MHC II binding of peptide to MHC class II peptides presented on plasma membrane |
| what isotype is not associated with a clear effector function? | IgD |
| which of the following does not apply to MHC class II molecules? | HLA-A, HLA- B, HLA -C |
| why is the peptide binding characteristics of MHC described as promiscuous binding specificity? | because it can bind with more than one antigen and this is important because then the MHC can present many more antigens to the T and B cells for an immune response |
| what is passive immunity? | immunity passed from one person to or a source to another person without the person having the original immune response. this happens with either breast feeding or immunization |
| explain the location and significance of immunoglobuliin CDRs (complement determining region)? | CDRs are made up of the hypervairable region looks of the variable regions of the BCRs, Igs, and TCRs -they make direct contact with the antigen thereby defining the specificity |
| Explain how naive B cell can simultaneously express both surface IgM and surface IgD, yet still display a single antigenic specificity | it can keep the same Fab region and go through a different RNA splicing for the Fc region. The keeps the antigen biding area the same while allowing the cell to have two different isotpyes of immunoglobulins on its surface |
| what are the distinguishing structural differences between chimeric, humanized and fully humanized monoclonal antibodies? | chimeric have the entire variable region from the mouse while humanized only have the CDRs. Fully humanized are made in cells of other species but using the human genes |
| where are dendritic cells always present? | in body tissues |
| when do dendritic cells become active? | with the uptake and degradation of pathogens and in the processing and presentation of their antigens on MHC type 1 and II moleucle s |
| Where do dendritic cells take up antigens from? | in the skin |
| Where do dendritic migrate to after they have taken up an antigen? | to the nearest lymph node where they settle in the T cell areas |
| What type of cells do dendritic cells activate in the lymph nodes? | naive T cells |
| What happens to to dendritic cells once they have activated naive T cells? | they mature and differentiate into mature dendritic cells |
| What type of dendritic cells are found in tissues? | immature dendritic cells |
| what causes the immature dendritic cell to migrate to the lymphnode? | expression of MHC II on surface and the chemicals it expresses (CCR7 & CCL21 are important) |
| What do CCR7 and CCL21 do to an immature dendritic cell? | cause migration of cells, stop antigen processing, focuses the cell to presenting antigens to naive T cells |
| What are the dendritic cells called which are in the lymph nodes? | mature or activated dendritic cells |
| What changes when a dendritic cell is activated? | the finger like projections become exaggerated and they have interaction with the T cells in the cortex of the lymph node |
| Can Macrophages move? | no |
| Can Macrophages interact with t cells? | no |
| how can Macrophages in the lymphoid tissues interact with other cells? | by ingesting something present that was carried there by the blood, lymph or extracellular fluid |
| What are the types of receptors does a dendritic cell have? | phagocytic, mannose, signaling, and toll like receptors |
| How does the dendritic cell get the antigen inside of it? | receptor mediated endocytosis |
| What cells do dendritic cells present to? | CDT4 with MHC class II |
| What do dendritic cells do with things not recognized by receptors? | macro pinocytosis |
| What does a dendritic cell do with a virus that infects it? | degrades the protein in the cytosol, brings proteins to the surface of the cell by proteasomes, and they are presented to naive CD8T cells by MHC I |
| What does a dendritic cell do with viruses that don't infect it? | they are presented through MHC I through cross presentation through the endocytic pathway |
| extracellular bacteria through receptor mediated endocytosis | MHC class II and CD4 T cells |
| extracellular bacteria, soluble antigens, and virus particles and macroinocytotsis | MHC class II and CD4 T cells |
| viruses with viral infection | MHC class I and CD8T cells |
| viruses and Cross presentation after phagocytic or macropinoocytic uptake | MHC class I and CDT8 cells |
| transfer from incoming dendritic cell to resident dendritic cell of viruses | MHC class I and CDT8 cells |
| What are the four types of adhesion molecules? | Vascular addressin, Selectin, Integrin, and Immunoglobulin like molecules |
| What is the chemical name of CD34? | vascular addressin |
| What is L-selectin? | Selectin |
| Where does selectin bind to? | on the surface of T cells to sulfated sialyl lewis carbohydrates of the vascular adressins on the surface of the high endothelial surface |
| what does LFA-1 stand for? | integrin |
| what does iCAM-1 stand for? | immunoglobulin like molecules |
| What does the combination of adhesion molecules do? | cause the naive t cells to slow down and attach to the high endothelial cells |
| What happens with the adhesion molecules when the T cell is attached? | strength is added through interactions between LFA-1 on the T cell surface and the adhesion molecules ICAM 1&2 on the vascular endothelium |
| What causes the CCR7 to keep holding tighter to the high endothelial cells | a constant supply of CCL21 and CCL19 |
| How do naïve T cells bind to dendritic cells in the lymph nodes? | transiently |
| how does the transient binding of T cells to dendritic cells in the lymph node work? | Through LFA-1 on T cells which bind to ICAM 1 and 2 and LFA 1 on the dendritic cells which bind on the ICAM3 on the dendritic cells and the DC-SIGN , this is strengthened by interactions between CD2 (on T cells) and LFA 3 on the dendritic cells |
| What happens to the T cell once it finds a compatible peptide:MHC on a dendritic cell? | It changes conformation of its LFA-1 so that it increases affinity for the ICAMs on the dendritic cell |
| How long does the conformational change of the T cell last? | Up to days to allow the T cells enough time to proliferate and differentiate |
| What makes co-stimulatory molecules? | Professional antigen presenting cells |
| Why are co-stimulatory molecules needed? | Because the presentation of peptide:MHC is not enough to activate the naïve T cell |
| What is CD28 known as? | A co-stimulatory signal |
| What are the ligands of CD28 structurally related to? | B7 molecules (B7.1 and B7.2) |
| What is needed for the proliferation and differentiation of naïve T cells? | B7 cells on professional antigen presenting cells, these engage CD28 on the cell surface, this allows the peptide:MHC compels to engage the receptors and co receptors on the same anitgen |
| What is CTLA-4? | It is a very similar to CD28, however it binds to the B7 about 20x more strongly, it has an opposite reaction than CD28 and represses proliferation instead of helping it |
| What are TH type T cells? | They are helper T cells made off of CD4 T cells |
| What are the cytokines which TH1 cells create? | IL-2, IFN-lambda |
| What do the cytokines of TH1 cells do? | Macrophage activation, B cell activation, production of opsonizing antibodies such as IgG1, inflammation |
| What are the cytokines of TH2 cells? | IL-4, IL-5 |
| What do then cytokines of Th2 cells do? | General activation of B cells to make antibodies, and lead to neutralizing antibodies |
| What are TfH cells? | Follicular helper T cells |
| Where are TfH cells found? | Found in secondary lymphoid tissues |
| What does TfH express? | CXCR5 which is the receptor for CXCL13, CXCL13 is made in B cell follicles |
| What do TfH cells do? | They produce IL-2 and help B cells |
| What does Th17 produce? | Large amounts of IL-17 |
| What is the development of Th17 based on? | IL-1 and IL-23 |
| What is the main function of TH17? | Pro inflammatory functions |
| What happens with too much TH17? | Rheumatoid arthritis, Cohn's disease, and psoriasis |
| What happens with too little TH17? | Job's syndrome and autoimmunity |
| What does the CD8T require for activation? | Stronger co-stimulatory activity than the CD4T cells |
| What can activate CD4T cells? | Only dendritic cells |
| What happens when a CD8T cells are activated? | They makes the cytokine IL-2 and the receptor, and these proliferation and differentiation of the cells |
| What can also activate CD8T cells? | CD4t cells, they have to recognize the same antigen on the same antigen presenting cell, it works because once the CD4T binds it secretes co-stimulatory functions and activates the CDT8 |
| How can the CD4T activate the CD8T? | Their simultaneously or sequentially |
| When will a CD8T only attack a infection? | When it is un-ambiguous because they often damage the tissue as well as killing or destroying the antigen |
| How do CTL's kill cells? | Though cytotoxins stored in lyric granules in cytotoxic effector ecells |
| When does the production of cytotoxins start for CD8T cells? | As soon as the T cell is activated & given a certain antigen, after that they migrate 2 the site of infection & look for the cells with the specific peptide:MHC complex and secrete the lytic granules on the surface of the cell & kill the cell by apoptosis |
| What does the lytic granule perforin do? | Causes apoptosis by making pores in the membrane |
| How does Fas killing work in terms of CTLs? | Causes the cell to go into apoptosis by using the Fas ligand to bind to the Fas molecule on the surface of the cells giving the cell the signal for apoptosis |
| What does Fas killing take care of outside of infection? | Unwanted lymphocytes |
| What is the wrong working of Fas killing? | Disease called autoimmune lymphoproliferative syndrome (ALPS) |
| What are Treg cells? | Regulatory auto reactive CD4T cells |
| What is the function of Treg cells? | To keep the activity of other effect or T cells in check and prevent autoimmunity, suppress the activation of naïve auto reactive CD4T and CD8T cytotoxic cells, to onto effect or T cells in the response to infection |
| What are the parts of the control effect or T cells in the response to infection of Treg cells? | A) make sure damage is limited b) make sure they are destroyed after the pathogen is gone |
| What are the characteristics of Treg? | Express high levels of CD25, the alpha chain of IL-2 receptors, FOx P3, make immunosuppressant cytokines: IL-4, IL-10 and TGF-beta, thought to respond by interacting with dendritic cells to take the other cells place |
| when can Treg cells cause a problem? | when they suppress things at the wrong time |
| what happens first in the activation of a b cell? | it is bound to a pathogen and then a signal is sent into the cell through Ig alpha and beta which change the gene expression in the nucleus |
| what needs to be given to the B cell to activate it? | co-receptors that are delivered to the cell when it becomes associated with another protein complex on the surface |
| What are the co-receptors for the B cell activation? | complementary receptor 2 (CD2 and CD21), CD19 and CD81 |
| What is the protein complementary receptor 2 (CR2 or CD21) | it is a co receptor for B cells and recognizes the iC3b and C3d breakdown products of the C3b fragments deposited on a pathogen |
| What is protein CD19? | B cell co receptor and act as the signaling chain of the receptor |
| What is protein CD81? | B cell co receptor which the function is not known, however we do know it does act as a cell surface receptor of Hep C |
| What do the CR 1&2 do on B cells? | these bind too the C3d fragments o the pathogen's surface which makes it susceptible to cleave by complement factor 1, both of these factors bind to the CR2, binding of the iC3b & C3d are the way that B recognize a pathogen |
| Which of the proteins activates the B cells in specific? | it is done by the phosphorylated tale of CD19 |
| what are T dependent b antigens | they need the T cell to recognize the protein they present and to have the cytokines that the T cell secretes as well |
| What are the two types of Thymus independent agents? | types 1 and type 2 |
| What are type 1 thymus independent agents? | these are used for the B cells to switch isotypes |
| What do the type 1 thymus independent agents need? | they activate B cells without a T cell or antigen and require more signals than produce by receptors & coreceptors , provided by TLRs, B cells only produce IgM when activated by them |
| what is the most common TLR type expressed by type one thymus independent agent? | type 9, can activate all of the 3 receptors and the B cell to differentiate and make antibodies, can make anti DNA antibodies because bacterial DNA becomes a TI-1 antigen |
| What is special about type 2 thymus independent agent? | made of repetitive carb or protein epitopes which are at high density, only stimulate b cells that are specific for antigens through cross linking, typical antigens are polysaccharides or pneumococcus, only early antibody response |
| What is specific about the type 2 thymus independent agent? | little or no isotype switching, almost all IgM, no somatic hyper-mutation |
| what is the first step in the full B cell response to the T dependent agent? | the dendritic cells present the circulating Tcells in the lymph node, w/ antigen specifc CD4T and MHC, this prompts the T cell to differentiate into helper t cells, the IL-4 in the node keeps some there as Th2 cells 2 activate antigen specific Bcells |
| what is the second step in the full B cell response to the T dependent agent? | the circulating b cells come into the lymph nodes through cytokines CCL21 and CCL19 |
| what is the third step in the full B cell response to the T dependent agent? | they enter the T cell zone through the afferent lymph node, start out in the T cell zone and are moved to the B cell zone by cytokines |
| what is the fourth step in the full B cell response to the T dependent agent? | the B cells moved into the Follicular dendritic cells and receive survival signals and leave the lymph node through the efferent lymph node |
| what is the fifth step in the full B cell response to the T dependent agent? | after this happens it next when it comes across a pathogen it will have a cross linking of the pathogen and co receptors starting a cascade of protiens |
| What happens in the cascade of proteins with a T cell activated B cell? | antigen gives signal 2 cell, the helper tcell binds 2 the Bcell & begins 2 synth cytokines/CD40 ligand, the recognition between B and T form cognate interaction and then the helper T cell reorients its cytoskeleton and secretory apparatus toward the Bcel |
| What is the first phase of B cell development? | repertoire assembly = generation of diverse and clonally expressed B cell receptors in the bone marrow |
| What is the second phase of B cell development? | negative selection = alteration, elimination of inactivation of B cell receptors that bind to components of the human body |
| What is the 3rd phase of B cell development? | positive selection = promotion of a fraction of immature B cells to become mature in the secondary lymphoid tissue |
| What is the 4th phase of B cell development? | searching for infection = recirculation of mature B cells between lymph, blood, and secondary lymphoid tissues |
| What is the 5th phase of B cell development? | finding infection = activation and clonal expansion of B cells by pathogen derived antigens in secondary lymphoid tissue |
| What is the 6th phase of B cell development? | attacking infection = differentiation to antibody secreting plasma cells and memory B cells in secondary lymphoid tissues |
| What is the order of phases of functional B cell development | repertoire assembly, negative selection, positive selection, searching for infection, finding infection and then attacking infection |
| What is the role of stromal cells in early B cell development? | provide specialized microenvironment for B cells at different times of development, make specific contacts with developing B cells through interactions of adhesion molecules and their ligands, and produce growth factors that act on attached B cells |
| What are stromal cells? | network of non lymphoid cells |
| What is the gene rearrangement that happens in early Pro B cells? | Heavy = D-J rearrangement L chain = germline no IG |
| What is the gene rearrangement that happens in late Pro B cells? | Heavy = V-DJ rearrangement L chain = germline No Ig |
| What is the gene rearrangement that happens in Large pre B cell? | Heavy = VDJ rearranged Light = Germline Ig = µ chain in endoplasmic reticulum |
| What is the gene rearrangement that happens in Immature B cells? | Heavy = VDJ rearranged Light = VJ rearranged Ig = µ heavy chain. Λ or κ light chain. IgM on surface |
| What is the definition of productive rearrangement? | rearrangements that preserve a correct reading frame and give rise to a complete and functional immunoglobulin chain |
| What is a non productive rearrangement? | gene rearrangements that do not translate into a useful protein |
| What is the function of a surrogate light chain? | to test an see if the µ heavy chain can combine with a light chain without using a light chain, instead lambda preB (mimics variable region) and lambda 5 mimics the constant region |
| How does B cell negative selection contribute to central tolerance? | it prevents B cells which react to the cells of the body from continuing in the maturation process and keeps the pathogen attacking ones in the maturation process |
| How does Bcell angery contribute to central tolerance? | this is where self attacking B cells are stunted and cannot produce IgM and only produce IgD, they cannot leave bone marrow, & only has half a half life of 1-5 days compared to the 40 days of a normal cell |
| What happens when a B cell are released from bone marrow and finds an antigen? | first they recirculate in the blood until they find a pathogen, then they migrate to te secondary lymphoid tissues where they mature to having high IgD and low IgM |
| What happens when a B cell is released from bone marrow and doesn't find an antigen? | they will ciruculate in the blood until coming into a secondary lymphoid tissue where they will develop so that when they encounter a pathogen they will bind, become plasma and start producing antibodies |
| What is the cellular organization of the thymus? | 1st epithelial cells arise frm ectodermal cells & medullary cells frm endodermal, 1st make thymic anlange, goes 2 multiple lobules which go into the medulla & cortex, cortex = immature thrombocytes, branched cortical epithelial cells and few macrophages |
| What is the organization of the medulla of the thymus? | mature thrombocytes, dendritic cells, and macrophages Hassall's corpuscles which are thought to be sites of cell destruction |
| What is the double negative phase of thymocyte development? | stem cells hv gone in2 the thymus which r not committed 2 the tcell lineage. after interacting w/ the stromal cells they are signaled to differentiate & divide causing the cells 2 loose their stem cell markers but do not hv any of the T cell markers |
| What is the double positive phase of thymocyte development? | this is when a thrombocyte proliferates and still expresses both CD4 and CD8. All the while the cell is determining where it will be alpha:beta or delta:lambda |
| What is the single positive phase of thymocyte development? | this is when the cell has finished developing and has either CD4 or CD8 not both and is alpha:beta or delta:lambda not both |
| What is the function of pre-TCR? | it is a checkpoint to make sure that the beta chain of the developing T cell has the potential to bind to alpha chains and if it can't the development of thymocyte is gone |
| What are the roles of thymic epithelial cells? | they interact very closely w/ the ++ thymocytes & help to turn the large ++ thymocytes into small double positive which the recombination machinery is reactivated and targeted to the alpha chain locus as well as to the y & d loci but not beta chain |
| What is thymocyte positive selection? | the name given to the process whereby that sm subpopulation is selected and signaled to mature further leaving the vast majority of double positive cells to die by apoptosis in the thymic cortex |
| What does thymocyte negative selection favor? | t cells that can recognize peptides presented by a self MHC molecule |
| What happens if a peptide MHC complex is bound within 3-4 days of the thymocyte expressing a functional receptor? | then a positive signal is delivered to the thymocyte which continues maturation, if not signal it dies |
| What will the thymocytes do that are chosen by positive selection? | the cells picked will becomes MHC restricted which means it will only bind to one type of peptide antigen in the context of that one MHC |
| What is thymocyte negative selection? | eliminates potentially auto reactive cells that could be activated by the peptides normally presented by MHC molecules on the surface of healthy cells |
| What shape are antibodies in? | y shape |
| Where are the heavy chains of antibodies? | lower stem and outer edge of the prongs |
| Where are the light chains of the antibodies? | inner sides of the upper prongs |
| What are the top and the bottom of an antibody connected by? | disulfide bonds |
| Where is the variable region on an antibody? | at the top of the prongs in the combination of the light and heavy chains |
| where is the constant region on an antibody? | on the bottom prong consisting of both of the heavy chains |
| Where is the Fab region of antibody? | the region that an antigen binds to at the end of the top prongs |
| Where is the Fc region of an antibody? | the constant region that doesn't change in the antibody, it is made of heavy chains |
| What are the major classes of human antibodies? | IgG, IgM, IgA, IgE, IgD |
| What is IgG? | dominant blood borne antibody that goes into the extracellular spaces within tissues and neutralizes microbial toxins and animal venoms |
| What is IgM? | first antibody to be produced, pentameric, and prevents blood borne infecton |
| What is IgA? | activated in the lymph nodes or spleen makes a contribution, protects the mucosal surface of the body and neutralizes microbial toxins and animal venoms |
| What is IgE? | mechanism for rapid ejection of pathogens from the body, bound with mast cells, creates allergies and asthma |
| What is IgD? | produced alongside IgM and tells the B cell when to activate |
| What is the framework region? | less variable regions flanking the hyper-variable regions, the rest of the looks and the beta strands |
| what is the hyper-variable region? | concentrated regions in variable regions, 3 found in each v region, the three loops that are farthest away from the constant region |
| What is antibody antigen interaction? | based on non-covalent forces, binding sites are rich in aromatic amino acids, each antibody binds to an antigen with different affinities, a good antibody is one that binds to an antigen and does no let go |
| What is an epitope? | the part of the antigen to which the antibody binds to, |
| What is a multivalent epitope? | having many epitopes |
| What is a linear epitope? | binds to parts of the antigen that are adjacent or in linear sequence |
| What is a conformational epitope? | epitopes that are separated but brought together by amino acid folding |
| What is germline configuration? | the original unrearranged organization of the Ig and T cell receptor genes in the DNA of germ cells and in somatic cells |
| what are the parts of the light chain? | VJ |
| What are the parts of the heavy chain? | VDJ |
| What are the steps of the recombination of the heavy and light chains? | it is directed by recombination signal sequence (RSS) which makes sure that the genes are connected in the correct order because there are different types of RSS that make it not possible for the different types of the chains to connect |
| What is the RAG protein? | made only in lymphocytes which r part of the V(D)J recombinase. RAG = recombination activating genes, the interact with each other & form the rag complex, then each of the diff complexes bind to diff Rss's and make a clean break, then it repairs the DNA |
| What does the RAG protein repair the DNA to? | it makes the coding joint |
| What is junctional diversity? | the adding of P and N nucleotides to the variable regions of antibodies |
| What are P nucleotides? | palindrome nucleotides |
| What are N nucleotides? | non-encoded nucleotides |
| How does the RAG protein work specifically? | The rag nicks the strand creating the P strand then the TdT (terminal deoxy nucleotidal transferase) adds N nucleotides and those bind together off of both strands, the unpaired ones are removed and the gaps are filled by DNA synthesis |
| What is allelic exclusion? | the process that makes sure only 1 heavy chain and one light chain are finally expressed so only a single antigen specificity is made |
| what is affinity maturation? | it is where the immune response to the pathogen continues and the antibodies have a higher and higher affinity for the pathogen |
| What causes affinity maturation? | somatic hyper mutation |
| What is somatic hypermuatation? | where with single nucleotide substitutions on the v regions of the heavy and light chains causing there to be a mutant immunoglobulin that can have a higher affinity for the pathogen and if they do they will be selected for |
| How does isotype class switching occurs? | a further DNA recombination where somatic recombined V region can be used with a different constant region, where the antigen specificity doesn't change but the constant region does |
| What is toxin neutralization in the terms of key antibody effector functions? | neutralizing antibodies which inactivate a pathogen or a toxin and prevent it from interacting with human cells. This happens in viruses by the neutralizing antibodies binding to the part of the virus which normally gains entrance to the cell |
| what is the blockage of pathogen colonization? | this happens with IgA on the outside of the body and keeps the pathogens from getting in, also happens through the skin, mucous membranes, and acidic surfaces |
| what is Opsonization? | happens with opsions and, this means coating the pathogen in immune system proteins to make them more easily ingested by phagocytes |
| what is complement activation? | can be done with an antibody bound to a bacterial surface and lead to the direct lysis of the bacterium |
| what is ADCC? | antibody-dependent cell-mediated cytotoxicity the killing of antibody coated target cells by NK cells having the receptor fcyRIII or CD16 which recognizes the Fc region of the bound antibodies |
| what is mast cell/ basophil activation ? | IgE is bound to mast cells and activated basophils which when they come across a pathogen they have a rapid release of inflammatory mediators |
| What are western blots | qualitative, semi quantitative id of a particular protein or a set of protein frm w/in a mix of proteins 1st they r separated by electrophoresis, then put on filter paper & exposed 2 the antibody of the protein of interest, the xtra antibody is washed off |
| What is the second half of western blots? | another antibody is added which will bind to the Fc region and turn it a color so that the actual area of the pathogen can be determined |
| what is immunoaffinity? | ths is used 4 the purification of the macromolecule, antibodies are put in beads in a column and then a mixture of macromolecules are put through the column and the ones which have affinity for the antibody will be stuck while the rest will pass through |
| What is chromatography? | looking at minute changes of color |
| what is immunoflorescent microscopy? | the use of antibodies that are conjugated to fluorescent molecules that gives off a distinct color that can be detected in a fluorescent microscope |
| what is FACS? | fluorescence activated cell sorting – cells linked with a fluorescent cell so that when the antibody connects with it the cell glows.These can be then ran through a flow cytometer and see exactly which cells were matched with the antibodies. |
| What are monoclonal antibodies? | made by taking bcells out of immunized animals, fusing them w/ tumor cells & making a hybridoma 2 create antibodies indef The diff hybridoma cells r then separated 2 make diff specificities of antibodies, these hybridomas make al Identical antibodies |
| how are humanized monoclonal antibodies made? | though genetic engineering, encoding CDR loops of the mouse monoclonal ab heavy and light chains replace those of a human immunoglobulin. thereby the ab are all human except for the CDR loops are of mouse origin |
| What are CDR? | complementarity determining region |
| how are humanized monoclonal antibodies being used as therapeutic drugs? | omalizumab = human IgE that is being assessed as a treatment for allergic asthma by binding to the constant region and keeping them from recruiting the inflammatory cells, also different ones can be used for rheumatoid arthitis |
| What is the variable region in terms of the TCR? | the top 1/3 of the protein which also houses the antigen binding site on top |
| What is the constant region in terms of the TCR? | the middle third of the protein that stays the same |
| what is the the CD3 complex of protiens? | Eta, delta, lambda, and zeta of the CD3 complex transduct the signal into the cell after the anitgen has been detected |
| What is the difference between alpha-beta (a-b) and lambda-delta (l-d)? | the d gene is situated w/in the a chain locus on c14 (btwn Va & Ja) & tht means when the a chain is rearranged the d gene is deleted & inactivated & in the l-d an xtra C chain can be added in allowing 4 more p & n nucleotides 2 b + 2 the recombined chain |
| What is the overall structure of the germline configuration of human TCR genes and the steps involved in VJ and VDJ recombination that result in a fully formed TCR? | happens the same way as the B cell except it happens in the thymus starts germline>recombination> rearranged DNA>transcription, splicing, transcription= t-cell receptor protein |
| What is the different between antigen recognition by TCR as compared to antigen recognition by antibodies? | antibodies can recognize a lg grp of epitopes frm protein, carb, fat & almost anything on the outside of a cell. However T cells can only recognize antigen's in the form of a peptide bound to an MHC |
| What is a CD8T cell? | cytotoxic and their main function is to kill cells that have become infected with a virus or some other intracellular pathogen, usually activated by a APC with MHC class I and then a secondary stimulation (CD28, 80) |
| What is CD4T cell? | (helper T cells) help other cells of the immune system to respond to extracellular sources of infection, and stimulate B cells to make antibodies and activate macrophages to phagocytize and kill pathogens plus secrete cytokines |
| What is a MHC I? | Major histocompatibility complex type 1, three alpha heavy chains the top two alpha 1-2 combine to form the peptide binding groove and alpha 3 is paired with a beta 2 microglobulin to support it |
| What is a MHC II? | Major histocompatibility complex type 2, made of two transmembrane chains one on either side consisting of alpha 1-2 (one side) and beta 1-2 (one side) and Beta & alpha 1’s combine to form the peptide binding groove |
| What do MHC I do? | they are presented to CD8 cells |
| What do MHC II do? | presented to CD4 cells |
| What do MHC I cells identify? | almost all cells of the body express this except for erythrocytes |
| What do MHC II cells identify? | expressed only on the cells of the immune system which specialize in the uptake, processing and presenting of antigens from the extracellular environment |
| What are the names of the human MHC class I molecules involved in antigen presentation? | HLA-A; HLA-B; HLA-C |
| What are the names of the human MHC class II molecules involved in antigen presentation? | HLA-DR; HLA-DP; HLA-DQ |
| What is the significance of MHC polymorphism? | o this is significant because most people inherit different polymorphics from each of their parents and they do not somatic recombine or mutate so it is needed to make people individual and to be able to bind to enough things |
| What does TAP stand for and what is it based off of? | transporter associated with antigen processing, based in the membrane of the ER and move peptides in cystolic processing of endogenous antigen and presentation they need ATP to work |
| What is the first step in cytosolic pathway? | ubiquitin, atp , and the proteasome complex which is associated with LMP2, LMP7 and LMP 10 are added to endogenous antigens |
| What is the second step in cytosolic pathway? | that makes peptides which are 8-13 amino acids long by exopetidases |
| What is the third step in the cytosolic pathway? | tap transports the peptides into the rough Er |
| What is the 4th step in cytosolic pathway? | the peptide encounters the MHC I complex and then is transported via the golgi body |
| What is the 5th and final step in cytosolic pathway? | the peptide is displayed on the cell surface |
| What is the purpose of the invariable chains? | to keep the alpha and beta binding cite from binding with peptides present in the ER, plus it is identical in all humans |
| What is the 1st step in the endocytic pathway? | An exogenous antigen is endocytosised or phagocytosised into the cell |
| What is the 2nd step in the endocytic pathway? | the MCH class II is broughout out of the golgi body after only the clip part of the invariant chain is left |
| What is the 3rd step in the endocytic pathway? | this is where the MHC II comes itno the endosome and HLA-DM removes the CLIP and allows the MHC II to bind |
| What is the 4th step in the endocytic pathway? | after the lysosome has digested the antigen and the MHC II is able to bind the 13-18 long amino acids |
| What is the 5th step in the endocytic pathway? | the MHC II peptide complex is displayed on the cell surface of professional and non professional APCs |
| What is the historical origin of immunology? | a. Practice of medicine b. Historical observations that people who survived the ravages of epidemic disease were untouched when faced with the same disease, they had become immune |
| What is a pathogen? | any organism with the potential to cause disease |
| What are the major types of pathogens? | bacteria, viruses, fungi, and internal parasites |
| What does the category internal parasites break down into? | it is used to signify a group of unicellular protozoa and multi cellular invertebrates (worms) |
| what is an extracelluar infection? | outside of the cells |
| What is an intracellular infection? | inside of the cells |
| How quickly does innate immunity work? | reacts quickly |
| How does the two part of innate immunity work? | recognition of a pathogen, response which includes effector mechanism which kill and eliminate the pathogen |
| What does innate immunity include? | complement |
| What does innate mean? | all determined by the hereditary genes |
| What does innate work to? | it works to slow the spread of infection |
| What does innate immunity calls upon what? | lymphocytes to increase strength |
| What is adaptive immunity? | lymphocyte reaction |
| How fast does adaptive immunity work? | much slower |
| How does adaptive immunity develop? | it develops against one pathogen |
| What does adaptive immunity provide? | a highly specialized defense that is of little use against infection by a different pathogen |
| What do the cell receptors of the adaptive immunity provide? | they are used by lymphocytes to detect pathogens |
| Is adaptive immunity genetic? | no |
| Is adaptive slow the first time? | yes because of primary immune repsonse |
| Is adaptive immunity fast the time? | yes it is a secondary immune response |
| What is Hematopoiesis? | the production of red and white blood cells |
| What are small lymphocytes? | production of antibodies or cytotoxi and helper T cells |
| What are plasma cells? | fully differentiated form of B cell that secrete antibodies |
| What are natural killer cells? | kills cells infected with certain viruses |
| What are neutrophils? | they do phagocytosis and kill microbes |
| What do esinophils do? | they kill antibody coated parasites through release of granule contents |
| What do basophils do? | they control immune responses to parasites |
| What do dendritic cells do? | activation of T cells and initiation of adaptive immune response |
| What do mast cells do? | they expel parasites from the body through the release of granules containing histamine and other active agents |
| What do monocytes do? | they are the circulating precursor cell to macrophages |
| What do macrophages do? | the phagocytize and kill microorganisms, they activate T cells, and initiate and immune response |
| What do megakaryocytes do? | platelet formation and wound repair |
| What do erythrocytes do? | oxygen transport |
| What does CD stand for? | cluster differentiation |
| What is a CD? | it is the macro molecule expressed on the outer layer of the cell |
| What is the most common function of the CD? | they are either receptors or signaling structures or as adhesion molecules that mediate cell-cell interatctions |
| What are the major types of cytokines? | interleukins (IL), Colony stimulating factors (CFS), Turmor Necrosis Factor (TNF), Transforming Growth Factors (TGF), Interferons (INF) and Chemokines = stimulate chemotaxis |
| What are the major lymphoid organs? | bone marrow, thymus, spleen, adenoids, tonsils, appendix, lymph nodes, and peyer's patches |
| What are the primary lymphoid tissues? | bone marrow, thymus |
| What do the the secondary lymphoid tissues do? | they are the cites where mature lymphocytes become stimulated to respond to invading pathogens |
| What are secondary lymphoid tissues? | anything outside of the thymus and bone marrow |
| What is lymph? | plasma collection, extracellular fluid, and has sluggish movement |
| What are the lymph nodes? | they collect the fluid, has b and t cell portions, and considered draining when has the fluid from an infected site |
| What is the spleen? | the lymphoid organ that servers as a filer for the blood |
| What is Malt? | more diffuse mucosal lymphoid tissue, and mucosa associated lymphoid tissue |
| What are the barriers to infection? | body surface, mucoual linings, skin, epithelial lining of the gut, stomach acid, mechanical, chemical and microbiological |
| What are the symptoms of an inflammatory response? | redness, swelling, heat , pain and loss of function is possible |
| What happens in an inflammatory response? | Mast cells & macrophages release mediators that stimulate capillary endothelial cells resulting in dilation of the capillary and an influx of fluid that causes the tissue to sell. The flow of blood to the region increases causing the redness and heat |
| What are the inflammatory cytokines? | IL-1, IL-6 and TNF-alpha |
| What is the process of phyagocytosis? | A pathogen is engulfed by a neutrophil or macrophage It has been marked 4 destruction c3b opsinization b. The neutrophil/macrophage engulfs it c. It is in a phagosome d. The granules of protein digesters/ membrane perforators tht destroy the cell |
| What is the physicality of defensins? | 35-40 peptides, righ in postively charged arginine residues, major human antimicrobial peptides, alpha and beta types, and amphipathic |
| What do defenins do? | destroy pathogens by penetrating the membranes and disrupting the integrity of them |
| Where is the alpha form of defensins most often found? | mainly expressed by neutrophils |
| What is the alternative pathway of complement activation?? | Pathogen surface creates local environment conductive 2 complement activation 1sr to act Complement activation Cleavage of C3 2 C3a & C3b, C3b covalently bound to surface components of pathogen Recruitment of inflammatory cells vi. Death of pathogen |
| What is the lethin pathway of complement activation? | Mannose binding lecithin bind to pathogen surface 2nd to act Complement activation Cleavage of C3 2 C3a & C3b, C3b covalently bound 2 surface components of pathogen Opsonization of pathogens , facilitating uptake & killing by pathogens Death of pathogen |
| What is the classical pathway of complement activation? | C-relative protein or antibody binds to specific antigen on pathogen surface Third to act Complement activation Cleavage of C3 to C3a and C3b, C3b covalently bound to surface components of pathogen Perforation of pathogen membrane Death of pathogen |
| What cytokine activates NK cells? | IL-12 produced by macrophages |
| What are NK cells apart of? | innate immunity |
| What do NK cells specialize in? | defense against viruses |
| What recruits NK cells to the site of infection? | IL-1 and TNF alpha made by neutrophils |
| What happens if NK cells are lacking? | persistent viral infections |
| What do NK cells secrete? | INF-lambda which activates macrophages which in turn activate T cells and B cells |
| What is the innate recognition of pathogens? | i. Pathogens have different things on their membranes which allow macrophages and other cytotoxic cells to recognize them as different and foreign |
| What are toll like receptors? | ii. Sense infection with a horseshoe shaped structure iii. Transmembrane polypeptide iv. Can have homo or heterodimers of TLR polypeptides v. Different kinds can be carried by different leukocytes and respond to different things |
| What are the differences between antibodies and TCRs? | a. Antibody i. Y shaped ii. Can be secreted iii. Called immunoglobulins iv. More variable b. TCR i. T cell receptor ii. Straight iii. Only work on membranes iv. Are never secreted v. Less variable |
| What are the general mechanisms by which diversity of antibodies and TCR are generated? | gene rearrangement and somatic recombination |
| Which of following events does not occur in the bone marrow? | rearrangement of TCR genes. |
| When a T cell binds to Ag/MHC presented by an APC that does not express B7, | the T cell becomes anergic |
| In MHC molecules, most variation in amino acids occurs | in the antigenic peptide binding groove |
| The activation of naïve CD8 T cells to become effector CTLs: | requires binding to B7 on dendritic cells is aided significantly by CD4 T cell secretion of IL-2 requires specific recognition of peptide antigen in MHC class I |
| Hematopoietic stem cells are | are self-renewing cells that give rise to all blood cell types |
| Which of the following is false regarding the function of the surrogate light chain? | Serves as a co-receptor in mature B cells |
| Which of the following does not apply to the thymus gland? | Th2 differentiation |
| True or False? In creating a functional TCR, the T cell uses the identical set of V, D, and J segments that the B cell uses in creating BCR, but the cells use different C segments. | False. Creation of functional TCR and BCR cells both happen the exact same way using the same process and proteins. but they do not use any of the same genes to do so |
| True or False? An individual with a deficiency in AID will likely be unable to produce IgG, IgA or IgE isotype antibodies. | true, AID is a protein that helps with isotype switiching. Thereby without the AID protein the cell cannot change the isotype of its immunoglobulins to be able to fight the infection more effectively. |
| True or False? A large complex protein antigen generally can combine with numerous different antibody molecules. | true. A large complex protein can combine with numerous different antibodies because it would have multivalent epitopes. |
| True or False? An immature B cell that readily binds to a bone marrow stromal cell will likely exit the bone marrow and migrate to a secondary lymphoid organ for further maturation. | False. It will probably not leave the bone marrow because it will be inactivated through negative selection due to its autoimmune response of binding to the bone marrow stromal cell. |
| True or False? Professional APCs can potentially activate both CD4 and CD8 T cells. | T can activate the CD4T cells normally & can activate CD8T cells through crossactivation where CD4T cells have bound w/ APCs&release cytokines & costimulatory cells which activate CD8T + express c 1&2 which allow interaction w/ both types of Tcells |
| In the ________ technique, antibodies are used to detect proteins previously separated by electrophoresis, whereas in the _______ technique, antibodies are used to detect antigens in micro-titer dishes. | western blot, ELISA |
| _______ expressed along with BCR and the ________ expressed along with TCR are said to be analogous in function, as they are both involved in relaying signal transduction events following antigenic stimulation. | BCR-Iga/Igb; TCR-CD3 |
| Following antigenic stimulation, phosphorylation of _________ relieves inhibition of the transcription factor _______, enabling it to enter the nucleus. | Ikb; NFkB |
| The lytic granules of CTLs contain _________ and _________. | perforin, granzymes |
| Following antigenic stimulation, __________ binds to phosphorylated _________ amino acid residues in the cytoplasmic tails of CD3. | zap70; ITAMs |
| Following antigenic stimulation, cleavage of phosphatidyl-inositol triphosphate phospholipids yields _______ and _______. | DAG, IP3 |
| Following antigenic stimulation, phospholipid derived _______ diffuses through the cytoplasm and induces release of _________ from the endoplasmic reticulum. | IP3 releases Ca+2 |
| In VDJ recombination, __________ proteins bind to _________ that follow the so-called “one-turn-two-turn” rule. | RSS; RAG |
| The prototypical Th2 derived cytokine, _________, induces B cells to switch to the ________ isotype, which has the capacity to sensitize mast cells and induce an inflammatory response. | IL-4; IgE |
| The _______ co-receptor binds to the beta-2 domain of _______ thus ensuring that helper T cells are stimulated by exogenous antigens. | CD4, MHC type II |
| Compare and contrast: Th1 versus Th2 (cytokines secreted and effector functions). | Th1 = IL-2, IFNg, inflammatory response and B cell activation Th2= lL-4 and IL-5, B cell activation, IgM with little isotype switching |
| Compare and contrast: NK cell versus CTL (one difference and one similarity). | NK cells are apart of innate immunity while CTLs are apart of adaptive immunity. NK cells and CTL cells both use lytic granules to destroy phagocytized cells |
| Compare and contrast BCR and TCR. Identify at least two similarities and two differences in both the structure and binding characteristics of these receptors. | similarities include: BCR and TCR similarities include: both have light and heavy chains, and both have a CDR/ variable region at the outward facing end which binds to a specific antigen. both contain two distinct chains |
| Compare and contrast BCR and TCR. Identify at least two similarities and two differences in both the structure and binding characteristics of these receptors. | differences: BCR and TCR differences include: BCR is in a Y shape while TCR is in a bar shape, and BCRs can be secreted as immunoglobulins while TCR are only on the surface of T cells. Both contain 2 distinct chains BCRs have two pairs while TCRs have 1 |
| What is allelic exclusion? When does it occur and why is it important? | Allelic exclusion is making sure tht the immunoglobulin only has 1 Isotype & specificity.Ths happens during maturation process of the Bcell. |
| An allergic reaction to poison ivy is associated with _____. | CTL activation |
| An example of type III hypersensitivity is _____. | serum sickness |
| Which one of the following types of immune responses is least beneficial in clearing helminth infections in the intestinal tract? | Th1 derived cytokines |
| The accumulation of variant HIV viruses that evade detection by memory B cells and T cells, and that develop resistance to drug regimes are attributed to | error prone reverse transcriptase |
| During the course of a successful desensitization process, the patient’s antibodies will change from an _____isotype to an _____ isotype. | IgE: IgG |
| Which of the following statements about M cells is false? | They process and present antigens directly to T cells. |
| Which description of HAART is false? | It is a cure for AIDS |
| Systemic anaphylaxis is typically triggered by the presence of allergen in _____. | the circulatory |
| What is Celiac disease? What is the immunological basis of this disease? | Celiac disease is where a person has a hypersensitivity to gluten. The M cell in the gut react to gluten and thereby cause an inflammatory response it. The symptoms of the disease can be alleviated through avoiding gluten. |
| What is the central argument proposed by the hygiene hypothesis? | is tht people hv become 2 clean & r not exposed 2 enough parasites & other allergens 2 hv the immune system react 2 them properly.with exposure to more parasitic worms & other pathogens when developing not have as many allergies or hypersensitivities. |
| Explain why individuals infected with HIV will typically experience a prolonged period of clinical latency. | Explain why individuals infected with HIV will typically experience a prolonged period of clinical latency. |
| what are whole organism vaccines? | The whole organism live attenuated is an organism that has been stunted to where it has limited growth and toxicity but best works to mimic a real infection. |
| What are whole organism live attenuated vaccines? | The whole organism live attenuated is when the organism has been treated to where it cannot reproduce or be toxic to the body but will cause the needed immune response. |
| Define seroconversion. | Seroconversion is where the amount of HIV virus is over a certain percent in the body fluids and tissues. This is when HIV turns into AIDS clinically. and generally a term applied to detection of serum antibodies to any antigen of interest |
| When an individual receives a kidney transplant, the concern will be to control the development of _____. | transplant rejection and allorecognition |
| Cancers develop their own blood supply and become vascularized through a process called _____. | angiogenesis |
| Chemical and physical agents that increase mutation rates by damaging DNA and increase the likelihood of developing cancer are known as _____. | carcinogens |
| Systemic distribution of cancer cells to other sites of the body through the bloodstream or lymph is a process known as _____. | metastasis |
| Which of the following is not considered to be an example of cancer immunotherapy? | radiation treatment |
| Which of these medical conditions can be treated by bone marrow transplantation ? | leukemia |
| What is a CAR-T cell? | CAR-T cells are chimeric antibody recognition T cells. These cells are coming of use in fighting cancer thorough making T cells with receptors perfectly matched for the tumors in the patient's body and placing them back in their body to fight the tumor. |
| Distinguish between preventative and therapeutic cancer vaccines. | Preventative target the virus so would involve anttenuated/inactivated virus as the vaccine; therapeutic would use tumor antigens |
| What is the rationale behind the use of anti-CTLA-4 and anti-PD-1 antibody therapies? | using anti-CTLA-4 and anti-PD-1 antibodies they are down regulators of T cells & when they bind to T cells they can stop them from working against the cancer these antibodies tht fight against the CTLA-4 and PD-1 keep the Tcells working against cancer |
| Briefly describe two distinctly different ways in which cytokines are used as cancer immunotherapies. | IL-2 is used to promote CTL activity GM-CFA and G-CFA are used to help people recover from the effects of chemo and radiation by helping their bodies to be able to produce more new blood cells and stifle the angiogensis of the tumors. |
| what is central tolerance | Central tolerance - the regulation and non-activation of auto-reactive B and T cells in the thymus and bone marrow by AIRE and different negative and positive regulation methods. a. AIRE b. negative regulation |
| what are the parts of peripheral tolerance | suppression, anergy, immunoprivlege |
| Where is the mucosal tissues of the body? | mostly in the trunk of the body and out of sight covered in thick secretions of mucus |
| What does the mucus surrounding the mucosal tissues always contain? | glycoproteins, proteoglycans, peptides, and enzymes |
| What does the composition of the the mucus help the mucosal tissue to do? | keep the epithelial cells from damage and limit infetion |
| Where does the mucosal epithelial line? | gastrointestinal tract, respiratory tract, urogenital tract, exocrine glands and many tissues |
| What exocrine glands does mucosal epithelial line? | pancreases, conjunctiva, lachrymal glands of the eye, salivary glands, mammary glands of the lactating breast |
| What tissues does the mucosal epithelial line? | gas exchange (lungs), Food absorption(gut), sensory activity (eyes, nose, mouth, and throat) Reproduction (uterus, vagina and breasts) |
| what are the secondary lymphoid tissues of the gut? | waldeyer's ring, palatine tonsil, lingual tonsil, adenoids, and in the intestines: preyer's patches and isolated lymphoid follicles |
| How are the strategies of mucosal immunity different from systemic immunity? | mucosal is different because it has a completely distinct set of lymphoid cells, hormones. and immunodulary factors, this response happens differently from that of the spleen, lymph nodes draining form the skin or muscles. |
| Why is the mucosal immunity different from that of systemic immunity? | because the mesenteric lymph nodes differentiate independently of the spleen and other lymph nodes |
| what is the role of commensal organisms of the digestive tract? | it is there to help the body develop the immune system so that as the person gets older they can fight off infections better compared to organisms which are born in germ free environments a d have low immune systems, low gut flora and have more infections |
| what is the role of M cells in the wall of the gut? | they help w/ adaptive immune responses by sampling gut contents & delivering material 2 pockets on the basolateral side of the Mcell membrane frm there dendritic cells & Bcells take up the antigen and stimulate the proliferation of antigen specific Tcells |
| describe lymphocyte circulation in the mucosal tissues? | main concept is tht the lymphocytes are activated in the mucosal tissues and thereby lose the homing mechanisms for the normal draining lymph nodes and only have the homing mechanisms to come back 2 the mucosal cells of any of the areas they are exposed 2 |
| how does the differentiation of mucosal tissue B and T cells start? | naive B & T cells which are circulating in the blood and mucosal routes are drawn into preyer's patches and mesenteric lymph nodes from the blood through high endothelial venules |
| What are the chemokines that draw the naive B and T cells into the preyer's patches? | CCL21 and CCL19 from the lymph organ |
| What do CCL21 and CCL19 bind to on the naive B and T cells? | CCR7 |
| What happens after the B and T cells are drawn into the Peyer's patches and they don't find an antigen? | it will be returned to blood ciruclation |
| What happens after the B and T cells are drawn into the Peyer's patches and they find an antigen? | it will be activated to proliferate and differentiate into effector and memory lymphocytes |
| What does the activation of B and T cells in the Peyer's cause? | activation causes the loss of CCR7, loss of cell adhesion molecule L-selectin, loss of being able to enter the secondary lymph nodes from the blood |
| What happens to the B and T cells after they have been activated in the Peyer's patches? | they leave in the lymph, travel via mesenteric and thoracic lymph nodes, and then back to the blood |
| What happens if they are activated in the mesenteric lymph nodes? | the leave in the efferent lymph and reach the blood |
| after the cells that were activated in the mucosal area how do they home back to it? | though integrin alpha 4: beta 7 which binds to addressin MAdCAM-1 which is found on the endothelial cell so the blood vessels of the gut wall |
| What guides the activated cell back to the mucosal tissue? | CCL25 which is secreted in the sm intestine and binds to CCR9 on the effector lymphocytes |
| When being guided by CCL25 how do they enter? | they enter through the laminia propria and plasma cells develop and make IgA and T cells activate intestinal macrophages |
| can the B and T cells activated in the mucosal tissues of the intestines home to other places? | yes |
| What does the function of being able to home to other mucosal tissues help with? | the antibodies of breast milk being from each different organ system |
| what happens if T cells are destined for intraepithelial lymphocytes? | they have a CCR9 chemokine receptor and express alpha E: Beta & and bind to E cadherin on the surface of epithelial cells allowing the cells to intercalcate within the later or intestinal epithelial cells while maintaining the epithelial barrier |
| what is the speed and strength difference between memory and regular B and T cells? | memory are much faster and stronger |
| Overall memory cells are more ______ than regular naive B and T cells? | susceptible to infection, easily activated, abundant for the same pathogen, have undergone isotype switiching and affinity maturation, produce more effective anitibodies |
| do memory cells go through somatic hyper maturation and affinity maturation again? | yes |
| what are memory cells derived from? | the highest affinity antibodies |
| how many more antibodies are created by the memory cells than the naive cells? | 10-100x |
| what do memory cells express more of? | MHC II |
| What is the time difference between the reaction time of a memory cell compared to a naive cell? | memory: 4 days naive: 8 days |
| what type of virus is influenza? | RNA virus |
| What happens the first time a person is infected with influenza? | primary immune response |
| How does influenza keep infecting people? | long term because it mutates into new viral stains that evade the proactive immunity generated during past epidemics |
| How many RNA molecules make up influenza? | 8 |
| What does an individuals immunity depend on? | The strain of virus they have had before |
| Who suffers the most with influenza? | those whose proactive immunity has been lost because of the new mutations of the current strain |
| What is it called with: those whose proactive immunity has been lost because of the new mutations of the current strain ? | antigenic drift |
| When does an almost new stain of influenza show up causing a pandemic? | every 10-50 years |
| What strains of influenza cause the worst pandemics recently? | avian flu |
| where do new strains of influenza often come from? | south east Asia where farmers live in close proximity to their animals |
| What is the theory of how new strains of influenza get started? | animals get infected with both human and their strain of influenza and then it recombines and jumps species |
| What is it called when influenza recombines and jumps species? | antigenic shift |
| What does trypanosomes do to evade the immune system? | change the proteins they show the immune system |
| How are trypanosomes transferred to humans? | through insect bites |
| Where do trypanosomes replicate? | in extracellular spaces |
| What is the surface of trypanosomes formed of? | glycoproteins that are encoded by over 1000 genes (VSGs) and only one of these proteins can be made at one time |
| How are the trypanosomes VSGs created? | through the rearrangement of the VSG by a process of gene converion |
| How does conversion of trypanosomes VSGs happen? | the expression site s excised, it is replaced with a copy of a different homologus gene,it will expressed a same dominant gene however a small percent will change the VSG that they express |
| What makes trypanosomes VSG deadly? | the immune system makes antibodies againist the dominanty forms killing them but allowing for the non dominanty forms to multiply |
| what does the cycling of trypanosomes/ parasite infections lead to? | heady deposition of immune complexes and inflammation which causes neurological damage and eventually leads to coma (sleeping-sickness) |
| What are the general mechanisms used by viruses to evade immune responses? | mutation, recombination, immune evasion (changing the proteins they present to the immune system), Gene conversion, and hiding form immune response otherwise known as latency |
| what is latency? | being inside a human cells without replicating, not making enough protein to have the cytotoxic CT8 cell respond, and does not cause dies |
| What happens when latency ends? | it will cause an episode of disease, which can happen when latency is broken by stress |
| what disease favors latency? | herpes virus |
| What does herpes virus do with the inhibition of humoral immunity? | virally encoded complement receptor that blocks the complement effector pathway |
| What does herpes virus do with an inflammatory response? | inhibits it |
| how does herpes virus block antigen processing and presentation? | inhibition of peptide transport by TAP and blocks peptide association with MHC class I |
| how does herpes virus immunosuprress the host? | virally encoded cytokine homolog of IL-10, inhibits Th1 lymphocyte, reduces IFN-lambda production |
| what does epstein barr virus do to evade the immune system? | takes over B cells and has latency |
| what does Mycobacterium tuberculosis do to evade the immune system? | commandeers the macrophage pathway of phagocytosis, prevents fusion of the phagosome with the lysosome, and then grows there |
| What does Listeria monocytogenes do to evade the immune system? | close to the same thing as the mycobacterium but it excapes the phagosome and grows in the cytosol, but since it grows there eventually CD8T cells terminate it |
| What is toxoplasma gondii? | a protozoan parasite |
| What does toxoplasma gondii cause? | toxoplasmosis |
| What does toxoplasma gondii do to evade the immune system? | creates its own special environment within the cells it infects, surrounds itself with membrane enclosed vesicles, this prevents the presentation of peptides to T cells |
| what does trepomena pallidum cause? | causes syphilis |
| What does trepomena pallidum do to evade the immune system? | evades antibodies by coating itself in human protiens |
| human cytomegalovirus does what as a virus? | it interferes with the expression of MHC class I molecules in many different was |
| human cytomegalovirus does what with US2? | targets the HLA class I molecules to the proteasome by transporting them to the cytosol |
| human cytomegalovirus does what with US3? | retains HLA class I in the endoplasmic reticulum blocking tasin fucntion |
| human cytomegalovirus does what with US6? | inhibits TAP ATPase activity and function |
| human cytomegalovirus does what with US10? | binds HLA class I and delays its departure from the ER to the cell surface |
| human cytomegalovirus does what with US11? | targets newly synthesized HLA class I heavy chains for degradation in the cytoplasm |
| human cytomegalovirus does what with US16? | inhibits NK cell recognition of infected cells by binding to the ULBP ligands of NKG2D |
| human cytomegalovirus does what with UL18? | MHC class I heavy chain homolog that binds to the to the NK cell receptor LILRB1 |
| human cytomegalovirus does what with UL40? | the leader peptide of ULU40 binds to HLA-E and subverys the ability of of CD94-NKG2A to monitor HLA-A, -B, - C expression |
| human cytomegalovirus does what with UL83? | blocks access to the proteasome and the generation of peptides for binding MHC class I |
| human cytomegalovirus does what with UL142? | downregulates the expression of the MIC-A and mIC-B ligands for NKG2D |
| why are live attenuated vaccines better? | because are they are better at protecting the immune response because they better mimic a real infection |
| how are live attenuate vaccines made? | by growing viral cells in non-human animal species |
| What are the major diseases treated by live attenuated vaccines? | Measles, mumps, sabin polio and yellow fever |
| how are the whole organism killed organism treated? | with formalin or physically treated with heat or radiation |
| What are the disease used in whole organism killed? | influenza, rabies, and salk polio |
| What are the type of organisms work for the whole organism killed? | only viruses with whose nucleic acids can be reliably inativated |
| What are the drawbacks of whole organism killed vaccines? | large amounts of pathogenic viruses are produced during the manufacturing process |
| What are subunit vaccines? | this uses the particular surface components of a pathogenic virus that the neutralizing antibodies |
| What is the problem with those who don't gain immunity from subunit vaccines? | they may lack an effective CD4 T cell response |
| What is a disease is prevented through the subunit vaccine? | Hep B |
| What is primary immunodeficency disease? | reveal themselves by enhanced susceptibility to infection or autoimmunity, Genetic, Usually in small culturally or geographically isolated groups and is X-linked |
| What is secondary immunodefeciency disease ? | not due to defective genes, from environmental factors, and usually died in infancy before 1940's |
| what causes aids? | HIV |
| What is AIDS characterized by? | by the massive reduction in the number of CD4T cells accompanied by severe infection of pathogens that rarely trouble healthy people |
| What type of virus is HIV? | an RNA virus with an RNA nucleoprotein core, surrounded by a lipid envelope and this envelope is derived from the host cell membrances |
| What is HIV retro virus? | called this because it uses an RNA genome to synthesize DNA intermediate (this is backwards from normal) |
| what can the proviruses of HIV be spread by? | CD4 T cells, dendritic cells, and macrophages |
| What can virions of HIV be spread by? | blood, semen, vaginal fluid, mothers mils, sexual intercourse, intravenous drugs, breast feeding or blood transfusion |
| What is the life cycle of HIV? | transfer to a person through exchange of bodily fluids, 1st infects a cell, viral integrase integrate the cDNA into the host genome to forma provius, the provirus uses the transcription and translation machinery of the cells to make new viral proteins, |
| What do the new viral proteins of HIV do? | become virions, which bind 2 CD4 & coreceptor on Tcell, viral envlope fuse with cell membrane and viral genome enters the cell, reverse transcriptase, copies viral genome into genome into 2x c DNA, viral cDNA enters the nucleus and integrates in2 host DNA |
| After HIV integrates into host DNA what does it do? | T cell activation induces some transcription of provirus, RNA transcripts are spliced to allow synthesis of the early proteins Tat and rev, tat amplifies transcription of viral RNA, viral RNA increase transport of RNA to cytoplasm, Gag, pol and ENV a |
| What happens with Gag, Pol and ENV in the HIV life cycle? | are made an assembled with viral RNA into VIrions which bud from the cell |
| What is HIV also known as? | a lentivirus because it is a slow progressing disease that can last for years and the immune system cannot terminate it |
| Explain how does the first infection with HIV works with the immune system? | it causes an immune response that creates HIV specific immune response by a HIV specific immune response |
| What happens when the HIV specific antibodies are made? | Cytotoxic T cells become activated to kill virus infected cells to reduce the virus load, and increase the number of circulating CD4T cells |
| What is seroconversion? | a detectable level of HIV antibodies in the blood |
| What is the correlation of the HIV and the subsequent disease? | the amount of virus that is left in the blood to the subsequent disease |
| what is the clinical latency of the HIV virus? | asymptomatic, 2-15 years, persistent infection of HIV and replication in CD4T cells causing a gradual decrease in the T cell numbers |
| when does the latency period end for HIV? | when the T cell count has become too high to make an immune response this marks the end of latency and the beginning of immunodeficiency/AIDs |
| what are non progressors? | where the HIV never comes out of laetnecy in some peopel |
| how many mutations happen in the HIV? | lots and lots |
| What does the reverse transcriptase lack? | a proofreading mechanism |
| what are the different types of HIV called? | quasi-species |
| What makes the HIV hard to get rid of in the immune response? | because of all of the variability |
| how does HIV not work with antiviral drugs? | because they can target it but then it mutates and the drugs cant target it |
| what is haart? | highly active anti-retroviral therapy |
| what haart in a therapy idea? | a combination therapy, to destroy the entire population of viruses before any one of them has accumulated enough mutations to resist all of the drugs |
| continuing with haart treatment does what? | slowly decreases the the virus until it is undecteable but not eradicated |
| What happens when you stop taking haart? | the virus comes back |
| what is the type one hypersensitivity Immune reactant? | IgE |
| what is the type two hypersensitivity Immune reactant? | igG |
| what is the type 3 hypersensitivity Immune reactant? | IgG |
| What are the type 4 hypersensitivity Immune reactants? | Th1, Th2 and CTL |
| What are the antigens for type one hypersensitivity? | soluble antigen (pollen) usually bound to IgE specific Fc receptor on Mast cell |
| what are the antigens for type 2 hypersensitivity? | cell/matrix associated antigen (binding to cell surface components) and cell surface receptors |
| What are the antigens for type 3 hypersensitivity? | soluble antigen |
| What are the antigens for type 4 hypersensitivity? | Th1 = soluble antigen (venom or peptide antigen) Th2 = soluble antigen CTL = cell associated antigen |
| What is the effector mechanism for type 1? | mast cell activation |
| What is the effector mechanism for type 2? | Complement FcR+cells (phagocytes and Nk cells) = cell or matrix association soluble antigen = antibody alters signaling |
| What is the effector mechanism for for type 3? | complement phagocytes |
| what is the effector mechanism for type 4? | th1 = macrophage activation th2 = esinophil activation CTL = cytotoxicity |
| what is an example of a type 1? | allergic rhinitis, asthma, systemic anaphyaxis (runny nose, breathing problems, or even death by asphyxiation) |
| What is an example of type 2? | some drug allergies (penicillin) = cell/matrix chronic urticarial (antibody to FαRIα = cell surface receptor |
| What is an example of type 3? | serum sickness, arthus reaction |
| What are examples of type 4? | th1 = contact dermatitis, tuberculin reaction th2 = chronic asthma, and chronic allergic rhinitis CTL = contact dermatitis |
| how does IgE bind to FcεRI with out an antigen in type one hypersensativity? | permanently |
| FcεRI (in type 1 hyper) is different how? | from B and T cells that once an antigen is present the cell starts working immediately |
| what type of receptor does FcεRI carry? | not just one type of IgE but many |
| What does FcεRI give protection against? | parasites |
| What are FcεRI usually stimulated by? | non-threatening substances |
| what do mast cells have expressed constitutively? | FcεRI |
| Where are mast cell present? | Epithelial tissues lining the body and all vascualrized tissues except a few |
| What vascularized tissues are mast cells not in? | central nervous system and the retina |
| what are the tasks of the mast cells? | maintain integrity of tissue, alert the local immune system to trauma and infection, and facilitate the repair for damage caused by the wound or infection |
| what is the cytoplasm filled with in mast cells? | 50-200 large granules of inflammatory mediators |
| What does mast cell mean? | in German = well fed or fattened cell |
| What do the granules contain? | histamine, heparin, tumor necrosis factor, chondroitin sulfate and neural protease |
| What does histamine do? | it is toxic to parasites, increases vascular permeability, and causes smooth muscle contraction |
| What does heparin do? | this causes the staining of mast cell granules with basic dyes, and other than that has the same function as histamin |
| What does tumor necrosis factor (TNF-alpha) do? | promotes inflammation, stimulates cytokine production by many cell types and activates endothelial cells |
| what are the two types of mast cells? | mucosal mast cells and connective tissue mast cells |
| what can only tissue mast cells do? | orchestrate IgE mediated allergic reactions through the release of inflammatory mediators (type 1) |
| When are mast cells activated in type 1? | with any antigen that can cross link with IgE bound to FcεRI |
| What happens after mast cells are activated in type 1? | degranulation happens within seconds |
| What are the three type of histamine? | types 1-3 |
| What does H1 (histamine) do? | binds to smooth muscle & endothelial cells on blood vessels, this causes vessel permeability, which causes inflammation and smooth muscle contration |
| What does the smooth muscle contraction of H1 cause in type 1? | coughing, sneezing, wheezing, vomiting, and diarrhea |
| what are the main things de-granulated in mast cell type 1 activation? | histamine, chymotrypase, trypase and other neural protease, activated metalloprotease in the extracellular matrix proteins |
| what is histamine complemented by in a type 1? | TNF-alpha |
| What does TNF-alpha do in a type 1? | activates endothelial cells, increases expression of adhesion molecules, promotes leukocyte traffic and makes more inflammation |
| The complement of histamine produces? | IL-4, TNF-alpha, and ecosaniods |
| What are excosanoids? | prosoglandins and leukotrienes |
| What are prostoglandins? | the promote dilation, increase permeability of blood vessels and are chemo attractant of neutrophils |
| What are leukotrienes? | like histamine but 100x more effective |
| What do mast cells attract? | eosinophils, basophils, neutrophils and Th2 lymphocytes |
| What does a mast cell do in terms of damage? | it kills parasites without mercy or regard to tssues damage |
| What does type 1 have to do with mast cells? | instead of putting all of this fighting against a parasite it does all of this against a harmless particle that only hurts the body in repsonse |
| What do Eosinophils have expressed constitutively? | FcεRI |
| What does activation of Eosinophils mean? | by external stimuli causes the release of toxic molecules and inflammatory mediators |
| What is the job of eosinophils? | to kill the invading microorganism or parasite directly |
| What do eosionophils secrete? | prostoglandins, leukotrienes, cytokines and MAJOR BASIC PROTEIN |
| What do the cytokines of eosinophils do? | amplify the inflammation, activation of epithelial cells and activation of more leukocytes including esinophils |
| What does MAJOR BASIC PROTEIN do? | causes the de-granulation of mast cells and basophils |
| Where is the production of eosionphils limited to? | production in the bone marrow |
| how are eosionphils activated | by Th2 and the production of IL-5 |
| What is the migration of eosionphils controlled by? | CCL5, CCL7, CCL11 (eotaxin) and CCL13 |
| What do all of the eosionphil migration chemokines bind to? | CCR3 |
| How do eosionphil contribute to the Type 1 problem? | they cause the airyway damage from chronic asthma |
| What do basophils do? | they initiate the Th2 repsonse through the secretion of cytokines IL-4, IL-13 |
| What do the basophil cytokines do? | activate Th2 |
| What do basophils do whenthey have been recruited to the infected site? | they are activated through toll like receptors and other receptors of innate immunity |
| What do basophils act most like? | eosinophil |
| Where are basophils recruited at the start? | to secondary lymphoid tissues that help with the polarization of the T cells towards the Th2 receptor |
| What do basophils express? | CD40 ligands |
| What does the CD40 ligand of the basophil bind to? | the CD40 of the B cells |
| What does the bound Basophil combine with to drive the isotype switching to IgE (in type 1)/? | IL-4 and Il-13 |
| What happens to the IgE after it is made by the in type 1? | it binds to FcεRI on basophils and provides a way for activating basophils in the secondary response |
| when is IgE favored in type I hypersensitivity? | when the immune system has a small amount of antigen and IL-4 is produced from CD4 T cells |
| What happens the first time allergen sensing is favored in type I hypersensitivity? | it is favored by production of antigen specific Th2 cells and cause the immediate de-granulation of the mast cells causing a wheal and flare reaction |
| What symptoms does IgE cause in the gastrointestinal tract in type I hypersensitivity? | violent musculus contractions, increased fluid flow, diarrhea and vomiting |
| What symptoms does IgE cause in the air ways in a type I hypersensitivity? | muscular spasms of the lungs, increased secretions of mucus and coughting |
| What symptoms does IgE cause in the blood vessels in type I hypersensitivity | edema, inflammation, increased lymph flow |
| what does Th2 do in a type I hypersensitivity? | CD4 T cells present antigens to Th2 cells and these are most often used because many allergens are proteases |
| What is localized anaphylaxis? | i. The immediate, transient kind of response that follows the injection of antigen (allergen) into the skin of a sensitized individual and is limited to the area surrounding the site of inoculation. |
| What is systemic anaphylaxis? | the widespread activation of connective tissue mast cells associated with blood vessels, disseminated mast cell activation, widespread constriction of smooth muscles, can cause anaphyactix shock |
| What is Anaphylactic shock? | blood pressure dropping suddenly due to the fluid leaving the blood, damage to organs, death through asphyxiation |
| Why does Anaphylactic shock cause death by asphyxiation? | because of swelling of airways and epiglottis |
| What can control an anaphylactic shock? | epinephrine which stimulates the re-connections of the tight junctions |
| What is the prevention method of treatment for type 1 hypersensitivity? | modify a patients behavior and environment to reduce allergen contact, allergen foods are avoided, pets are kept outside, houses are redone to make mites less prevalent, desert vacations or sea cruises are taken during pollen season |
| What is the pharmacological treatment for type I hypersensitivity? | the use of drugs to reduce the impact of contact with allergens, drugs that block effector pathways, limit inflammation after IgE, antihisamies, corticosteriods, Cromolyn sodium and Epinephiine |
| What is the immunological treatment for type 1 hypersensitivity? | to prevent the production of the allergen, the goal is to switch from IgE to igG using a process of desensitization = allergen injection, small to large, because IgG4 is monovalent it forms complexes with the antigen that no not recruit effector cells |
| What is the problem with the IgE-IgG form of immunological therapy for type 1 hypersensitivity? | it can cause anaphylaxis |
| What is the more modern approach to immunological therapy for type 1 hypersensitivity? | the goal is to induce anergy of allergen specific T cell in vivo by decreasing the expression of CD3:T cell receptor complex at the Th2 cell surface , there is very very little chance that it could trigger anaphyxis |
| the hygiene hypothesis | we are too clean and thereby are not exposed to enough chronic infections of parasites or microorganisms and thereby we have a hypersensitivity to type 1 allergens |
| what does type II hypersensitivity use to make a response? | epitopes that stimulate the formation of IgM and IgG antibodies that are specific for the conjugate drug and cell surface componet |
| how can type II hypersensitivity best be described? | as antibody mediated cytotoxicity with cell death occurring by ADCC or by complement mediated destruction. These reactions are triggered when cell surface structures are chemically modified or recognized as non-self by the immune system |
| what happens with type II hypersensitivity and penicillin and blood transfuction? | penicillin modified blood cells acquire a coating of the complement compound C3b as a side effect of complement activation for a bacterial infection, this facilitates phagocytosis by macrophages, these process the modified penicillin protein |
| After macrophages process the modified penicillin protein in a type II hypersensitivity including blood transfusion and penicillin? | they present the protein to specific CD4T cells which are activated to become Th2 cells, these stimulate antigen speicific B cells to produce antibodies against the penicillin modified epitope, binding of these antibodes causes complement |
| in type II hypersensitivity what type of pathway is is completed in a penicillin and blood transfusion situation? | the classical pathway which results in cell lysis by terminal complement components and receptor mediated phagocytosis |
| what is the general mechanism and consequence of type III hypersensitivity? | a. Type III hypersensitivity occurs when IgG antibodies bind to soluble antigens and form complexes that activate the complement cascade. The local inflammatory response that is triggered by complement activation is responsible for the clinical symptoms` |
| What is the arthus reaction of type III hypersensitivity? | usually appears as localized areas of erythema and hard swelling that usually subside within the day, they can usually be found at the site of injections of allergens in the use of the desensitization method |
| what is the immune response in the arthus reaction of type III hypersensitivity? | immune reaction in the skin caused by the injection of antigen into the dermis. the antigen reacts with specific IgG antibodies in the extracellular spaces. this activates the complement and phagocyitic cells to produce a localized inflammatory response |
| What does the arthus reaction depend on in type III hypersensitivity? | the Fc receptors and does not occur in mice without the lambda chain that is common in all Fc receptors |
| What type of hypersensitivty is serum sickness associated with? | type III hypersensitivity |
| What are the collection of symptoms of serum sickness caused by in type III hypersensitivity? | they come following the injection of large amounts of foreign molecule into a person, it is cause by the immune complexes formed between the injected protein and the antibodies that are made against it, |
| When does serum sickness happen? | 7-10 days after injection |
| What are the symptoms of serum sickness | chills, fever, rash, arthritis, vasculits, glomerulonerphritis |
| When does onset of serum sickness happen? | when the synthesis of antibodies which form immune complexes attack the percieved antigen and activate complement which causes great damage |
| What happens if the same antigen is given again in serum sickness? | it will come back much worse |
| When is serum sickness often found today? | with the treatment using monoclonal antibodies, myocardial infarction (with the treatment of the bacterial enzyme streptokinase ot degrade blood clots) and intravenous admin of drugs such as penicillin |
| What do type IV hypersensitivities reactions involve? | effector T cells instead of antibodies |
| How does a type IV hypersensitivity reaction happen? | an antigen is placed int he subcutaneous tissues and processed by local antigen presenting cells, a Th1 effector cell recognizes antigen and releases cytokines which act on vascular endothelium, recruitment of T cells, phagocytes, fluid and protein 2 site |
| What happens in a type IV hypersensitivity when stuff is recruited to the site? | it causes a visible lesion between 24-72 hours of contact |
| How does a tb test give an example of type IV hypersensitivity | small amt of cell wall placed intradermally, patient is examined 24-72 hours later, fomentation of a red raised bump due to migration of memory Th1 cells and macrophages and shows that there has been a previous exposeure ot the pathogen |
| What is a problem with the tb test in type IV hypersensitivity? | it can be a false positive if they have been previously immunized with BCG |
| How does poison ivy go along with type IV hypersensitivity? | causes contact sensitivity, involves CD8T and Th1 cells, the chemical that causes the reaction is pentadecacatechol that covalently attaches to extracellular and cell surface proteins to form neoantigenic structures, apcs then present |
| where are CD4 and CD8 T cells presented in the type IV hypersensitivity case of poison ivy? | modified self antigens, the clinical symptoms include- blistering skin, inflammatory blood cell infiltration |
| What is celiac disease in terms of type IV hypersensitivity? | it is genetic and environmental, often a person makes igG or IgA against gluten, it is an autoimmune disease, 1-133 people have it, inheritance of MHC II HLA_DQ8 or HLA-DQ2 inflammation of sm intestine caused by activation of CD4T cells |
| What is central tolerance in its simplest form? | the (-) selection of B and T cells to eliminate the lymphocytes bearing self reactive receptors before they go into circulation, this happens during delvelopment, it also invloved the AIRE protein which is a transcription factor expressed on thymic APC's |
| what is the disease where a person is deficient in AIRE? | a multi-organ autoimmune disease called Autoimmue Polyendocrinopathy Candidasis Ectodermal Dystrophy APECED which is characterized by immune attacks targeting the endocrine glands |
| What is peripheral tolerance? | it refers to tolerance mechanisms that act outside of the bone marrow and the thymus glands specifically: immune privilege, anergy and suppression |
| What is immune privilege in peripheral tolerance? | several rogans of the body that are shielded from the immune system |
| What organs are in immune privilege? | central nervous system, eyes, testes and uterus during pregnancy |
| What is suppression in peripheral tolerance? | it is mediated by the action of suppressive cytokines such as LI-10, TGF-beta and the action of regulatory T cells |
| What is anergy in terms of peripheral tolerance? | the induction of a frozen state upon auto reactive B cells or T cells |
| are any autoimmune diseases caused by type one or IgE hypersensitivity? | no |
| What are type 2 hypersensitivity autoimmune diseases? | caused by anitbodies directed against cell surfaces or the extracellular matrix, often directed at blood and is an example of autoimmune hemolytic anemia |
| what are type 3 autoimmune diseases ? | they are caused by soluble immune complexes deposited in tissues |
| What are type 4 autoimmune diseases ? | caused by effector T cells |
| What is the autoimmune disease autoimmune hemolytic anemia hypersensitivity type? | type 2 |
| What is autoimmune hemolytic anemia ? | a reduction of red blood cells through phagocytosis or lysis of red blood cells |
| how are blood cells lysed in autoimmune hemolytic anemia ? | by IgG and IgM binding to them and starting the classical complement pathway which ends in cell lysis |
| how are blood cells killed by phagocytes in autoimmune hemolytic anemia ? | they are coated with antibody and C3b and cleared form circulation by Fc receptors and complement receptors on phagocytes in the spleen |
| What is a treatment of autoimmune hemolytic anemia? | splenectormy which reduces the rate at which the cells are opsonized and it works because the blood cells are still able to function with a bound antibody complement structure |
| What are the auto-antigens of autoimmune hemolytic anemia ? | Rh blood group antigen, I antigen |
| What type of hypersensitivity is Grave's disease? | type 2 |
| what is the autoantigen of Grave's disease? | thyroid stimulation hormone receptor |
| What is the consequence of Grave's disease? | hyperthyroidism |
| What are the symptoms of Grave's disease? | heat intolerance, nervousness, irritability, warm moist skin weight loss, enlargement of the thyroid |
| What are the symptom's of Grave's disease caused by? | antibodies bound to the TSH receptor |
| What does Grave's disease cause? | a chronic overproduction of hormones outside of regulation and metabolic needs |
| What are the obvious symptoms of Grave's disease? | bulging eyes and characteristic state |
| What response does Grave's disease tend toward? | CD4 and Th2 |
| What is the treatment of Grave's disease? | drugs that inhibit thyroid production short term long term- removal by surgery, destruction by uptake of radioisotope 131 I and is followed by daily dose of thyroid hormone |
| What is Hashimoto's disease? | chronic thyroiditis or a thyroid that cannot make hormone |
| What does Hashimoto's disease involve? | a CD4/ Th1 response with both antibodies and effector T cells specific for thyroid antigens are produced making lymphocytes come to the thyroid to destroy it and make the person hypo thyroid |
| What are the treatments of Hashimoto's disease? | replacement therapy and thyroid and hormones taken on a daily basis |
| What is a feature of Hashimoto's disease? | ectopic lymphoid tissues |
| What are the ectopic lymphoid tissues of Hashimoto's disease? | they look like secondary lymphoid organs within the thyroid, are formed by lymphoid neo-genesis, and are also called tertiary lymphoid organs |
| What type of hypersensitivity is type one diabetes? | type IV |
| What is the auto-antigen of type one diabetes? | pancreatic beta cell antigen |
| What is the consequence of type one diabetes? | beta cell destruction |
| When does type one diabetes usually start? | childhood or adolescence |
| Why do the symptoms take so long to show up? | because when it starts the body has many more insulin producing cell than it needs |
| What is the treatment of type one diabetes? | daily infection of purified pig or recombinant human insulin however the pig insulin can cause serum sickness and lead to tissue damage |
| What type of autoimmune disease is lupus? | a systemic autoimmune disease which is also a chonic inflammatory disease |
| What is the chronic inflammatory part of lupus? | binding antibodies to cell complexes, when destruction happens it adds more material for the immune system to react against, |
| what type of hypersensitivity is lupus? | type 3 |
| What is the auto-antigen of lupus? | DNA. histones, ribosomes, snRNP, and scRNP |
| What are the consequences of lupus? | Glomerulonephritis, vasculitis, arthritis, butterfly rash |
| What population is lupus common in? | African and Asian women |
| Why is this disease cause lupus ? | a wolf like appearance |
| What are common sites of lupus inflammation? | joints which can cause arthritis |
| What type of hypersensitivity is rheumatoid arthritis? | type IV |
| What is the auto-antigen of rheumatoid arthritis? | unknown synovial joint antigen |
| What is the consequence of rheumatoid arthritis? | joint inflammation and destruction |
| What is sometimes part of rheumatoid arthritis? | ectopic lymphoid tissues |
| What is rheumatoid arthritis sometimes caused by? | lupus |
| what percentage of the American population does rheumatoid arthritis effect? | 1-3% |
| when does rheumatoid arthritis usually start? | 20-40 |
| What does rheumatoid arthritis stimulate B cells to produce? | IgM, IgG, IgA which are all specific for the Fc Region of IgG and all called rumatoid factor |
| when joints are infected by rheumatoid arthritis the leukocytes that infiltrate are? | CD4T which secret pro-inflammatory mediators (IL-1&6 and TNF alpha), CD8 T, B cells, Lymphoblasts, Plasma cells ( make rheumatoid factor), neutrophils (release lysosomal enzymes which cause tissue destruction) and macrophages |
| what are the treatments of rheumatoid arthritis? | physiotherapy, anti-inflammatory drugs, Immunosuppressants, infusion of anti-TNF alpha monoclonal antibodies and use of anti-CD20 antiboidy |
| What is the Infusion of anti-TNF alpha monoclonal antibody treatment of rheumatoid arthritis? | called infliximab, eliminates the cytokines, reduces inflammation, joint pain and joint swelling |
| What is the treatment of anti-CD20 antibody? | rituximab, depletes B cells through ADCC to 2% |
| what is the hypersensitivity type for multiple sclerosis? | type IV |
| What is the auto antigen for multiple sclerosis? | myelin basic protein, proteolipid protein (the myelin sheath around nerve cell axons) |
| What are the consequences of multiple sclerosis? | brain degeneration and paralysis, motor weakness, impaired vision, lack of coordination, spasticity, occurs in late 20s-30 and has a highly variable rate of decline |
| what do TH1/CD4 do in multiple sclerosis? | they secret interferon lambda and enrich the blood and cerebrospinal fluid |
| where are activated macrophages in multiple sclerosis? | they are present in sclerotic plaque and release proteases and cytokines which cause direct de-myelination |
| What is a characteristic of multiple sclerosis? | ectopic lymphoid tissues |
| Where are sclerotic plaques formed in multiple sclerosis? | the white matter of the central nervous system |
| what is the treatment of multiple sclerosis? | regular subcutaneous injections of IFN beta1 and high does of immunosuppressive drugs which reduce attacks and plaque formation |
| What hypersensitivity is myasthenia gravis? | type II |
| what is the auto-antigen of myasthenia gravis? | acetocholine receptor |
| What are the consequences of myasthenia gravis? | progressive weakness as the loss of receptors makes the cell much less sensitive to neuronal stimulation, droopy eyelids, double vision, weakened chest muscles, and impaired vision |
| What are the treatments of myasthenia gravis? | pyridostigmine = inhibits the enzyme cholinterases azathioprine = inhibits the production of autoantibodies |
| What are genetic factors that make people more prone to autoimmune disease? | genetic, environmental, physical trauma, infection |
| What are some of the different genetic things that can go wrong? | absence of transcription factor AIRE, Absence of FoxP3 in Treg cells, IPEX, dys-regulation of CTLA-4 in terms of T cell costimuatino, and HLA genes |
| What is the absence of AIRE linked to nation wise? | Finns, Sardinians and Iranian Jews |
| What does the absence of FoxP3 in Treg cells do? | it happens mostly in boys, the gut is almost always effected and usually the thyroid, pancreatic B cells and the skn |
| What does IPEX stand for? | Immune dys-regulation, polyendocrinopathy,enteropathy, and X linked syndrome |
| What does the genetic HLA pre-disposition have to do with autoimmune disease? | usually in type I or II HLA, more often in type II, there is no such thing as a good or bad allele in HLA allotypes except HLA-B27 which almost always causes akylosing spondylitis |
| what are the environmental things that can cause autoimmune diseases? | smoking, physical trauma, infection/molecular mimicry, less production of naïve T cells and maybe the hygiene theroy |
| How does smoking cause autoimmune diseases? | damaged alveoli of the lungs exposing the basement membrane to antibodies and deposition of tissues |
| How does physical trauma cause autoimmune disease? | example eye: the body will send active T cells for the burst one and to the healthy one causing an autoimmune response to the healthy eye that can cause blindness |
| What are the types of molecular mimicry? | rheumatic fever or bacterial infection |
| What is the definition of molecular mimicry? | Antibodies produced to defeat infections can also fight against heart tissues that have structurally similar epitopes |
| What are the strategies currently in use and development and treatment of autoimmune disease? | immunosuppressive and anti-inflammatory agents, the blocking of anti-inflammatory cytokines, the blocking of activation and infiltration of T cells and humanized monoclonal antibodies |
| What are the major challenges that underlie organ transplantation? | major points of rejection are MHC and HLA because they are highly polymorphic, organ shortage, rejection, destruction of healthy tissues |
| What are major clinical problems in organ transplantation? | transplants must b introduced in a way tht allow them 2 preform normal function, health of recipient & transplant must b maintained during transplanting & surgery, immune system of the patient must be prevented from developing detrimental immune response |
| what are alloantigen's? | antigens that vary between members of the same species |
| What are the two types of allorecognition? | transplant rejection and graft vs host reaction |
| what organs does transplant rejection usually come from? | Kidney, heart |
| What types of transplant rejection are there? | Hyper acute rejection, and acute rejection |
| What is hyper acute rejection in transplant rejection ? | it is directly comparable to type III hypersensitivity, to avoid it donors and recipients are typed and cross matched for the ABO blood groups and antigens |
| Where do the HLA antibodies come form in transplant rejection ? | pregnancy, blood transfusion, and previous transplants |
| What is acute rejection in transplant rejection ? | it is like type IV hypersensitivity and the alloreactive T cell responses produce CD4 and CD8 T cells both of which can attach the organ graft and destroy it there are two pathways of this |
| What are the pathways of acute rejection in transplant rejection? | direct/ indirect and chronic rejection |
| What is the direct pathway of acute rejection in transplant rejection ? | produces effector T cells that move to the transplanted tissue, Th1 cells activate resident macrophages which cases inflammation and CD8T cells kill the transplanted tissues |
| What is chronic rejection (indirect pathway of allorecognition) in acute rejection in transplant rejection ? | this happens months or years after the transplant, it is characterized by reaction in the vasculature of the grat that causes thickening of the vessel walls and narrowing of the lamina, graft dies as the blood supply is cut off through ischemia and |
| What cells cause chronic rejection in t transplant rejection ? | CD40 ligands on the B and helper T cells |
| What is the graft vs host reaction in transplant rejection ? | usually happens with bone marrow transplant, arises from mature T cells in the grafted bone marrow, these attack and reject the recipient's healthy cells, this happens to varying degrees in almost all recipients of bone marrow transplants |
| What are corticosteroids? | anti-inflammatory agents |
| What corticosteroid are people usually given? | prednisone, it is a pro-drug and it becomes active once inside the bod |
| How are corticosteroids produced? | natural form human glucocorticosteroids |
| What do glucocorticosteroids do? | act as negative regulatory agents, down regulate inflammatory response, alters homing of lymphocytes, increases production of IkappaB alpha and decreases production of NFkappa B |
| What are the side effects of corticosteroids? | fluid retention, weight gain, diabetes, and thinning of bone and skin tissues |
| What do cytotoxic agents do as a immunosuppressive therapy? | inhibit cellular proliferation, inhibit activation of adaptive responses and also commonly used to treat cancer |
| Which cytotoxic agents are usually used as immunosuppressive? | azathioprine, cyclophosphamide, methotrexate |
| what does azathioprine do as a cytotoxic agents ? | inhibits the production of inosinic acid which is a component of DNA, however does damage all healthy cells that are active in cell division |
| What tissues are effected by azathioprine as a cytotoxic agents ? | bone marrow, intestinal epithelium, hair follicles, leads to anemia, leukopenia, thrombocytopenia, intestinal damage, hair loss and fetal development is adversely effected |
| What is cyclophosphamide as a cytotoxic agents ? | mustard gas, used before or after antigenic stimulation, damages: bladder, cancer causing and causes hemorrhagic cystitis. however it does not damage the liver |
| What does methotrexate do as a cytotoxic agent? | treats cancer, prevents DNA replication and is the drug of choice for inhibiting G vs HD in bone marrow transplant |
| What is the major side effect of all cytotoxic agents? | risk for opportunist infection, and toxicity |
| what are T and B cell activation inhibitors? | they block signaling moelcues that are part of the transduction pathway |
| What are the main types of T and B cell activation inhibitors? | cyclospoin A and tacrolius, rapamycin |
| What does cyclospoing A and tacrolius do? | blocks calcieurin |
| What does the blocking of calcineurin cyclospoing A and tacrolius do? | disrupts activation by blocking the transduction signal from the T cell receptor |
| What does rapamycin do? | it inhibits T cell activation by blocking IL-2 |
| What are patients at risk for by using T and B cell activation inhibitors? | opportunistic infections and drug induced organ toxicities |
| What is the effect of calcineurin cyclospoing A and tacrolius on T lymphocytes? | a. Reduced expression of IL-2, Il-3, IL-4. GM-CSF, and TNF a b. Reduced cell division because of decreased IL-2 c. Reduced Ca+2 dependent exocytosis of cytotoxic granules d. Inhibition of antigen driven apoptosis |
| what is the effect of calcineurin cyclospoing A and tacrolius on B lymphocytes? | a. Inhibition of cell division because T cell cytokines are absent b. Inhibition of antigen driven cell division c. Induction of apoptosis after B cell activation |
| What is the effect of calcineurin cyclospoing A and tacrolius on granulocytes | reduced Ca2+ dependent exocytosis of granules |
| How are humanized monoclonal antibodies used as T and B cell activation inhibitors? | against CD3 and IL2 receptors they are approved for use however they still leave the patient open to opportunistic infections and other side effects |
| what are bone marrow transplants used for? | to provide hematopoietic stem cells from a healthy and matched donor in order to replace the recipient's blood cells/ entire hematopoietic system with those of the donor |
| How is a bone marrow transplant done? | bone marrow from the donor is removed by needle aspiration and transferred to the recipient by injection into the bloodstream. Previously the recipient will have undergone chemotherapy & radiation treatments to remove diseased cells. |
| What are the symptoms of graft vs host disease? | 10-28 days after transplantation, fine diffuse erythematous rash (palms of hands, soles of feet, head, and then spread to trunk) and intestinal reaction causes: cramps, diarrhea, inflammation of the bile ducts and rise of liver enzymes in the blood |
| graft vs host disease can be caused by what? | bone marrow transplant that has a non matched HLA donor |
| what happens immunologically in graft vs host disease? | T cells of donor origin attack the recipient's tissues. In graft-versus-host disease, mature donor leukocytes that are present in the bone marrow can mount an attack against the recipient's tissues. |
| what is the book definition of cancer? | disease that are caused by abnormal and invasive cell proliferation |
| what do cancer cells resemble? | virus infected cells in that their internal affairs have been perturbed and reordered from these of normal cells |
| What are the 6 characteristics of cancer? | i. Stimulate their own growth ii. Ignore growth inhibiting signals iii. Avoid death by apoptosis Develop a blood supply Leave their site of origin to invade other tissues Replicate continuously 2 expand their number outrun the immune response |
| what are benign tumors? | warts, encapsulated, localized, and limited in size |
| what are malignant tumors? | continually increase in size, can break through basal laminae and invade adjacent tumors |
| What is metastasis? | the spread of a tumor from its site of origin to other tissues some cells from the primary tumor invade other tissues and grow and divide to become secondary tumors |
| What are the classes of carcinogens? | chemicals, ultra violet light, radiation, smoking, oncogenic viruses |
| What types of cancerous mutations do chemicals tend to cause? | single nucleotide substitutions in DNA |
| What cancerous mutations do radiation cause? | DNA breaks, cross linked nucleotides, abnormal recombination, chromosomal translocation |
| What causes lung cancer? | smoking |
| What do oncogenic viruses effect? | all but one DNA |
| What is the RNA retro-virus? | HTLV-1 or adult T cell leukemia |
| What are the types of mutations caused by oncogenic viruses? | the taking over of cells and making novel DNA uncontrolled replication OR viral proteins bind to p53 and tumor suppressor protein called Rb blocking their functions and enabling the virus infected epithelial cells to proliferate |
| What is DNA papilloma virus? | benign wars, carcinoma of the cervix and its found worldwide |
| what is hep B virus? | liver cancer that is usually found in Southeast Asia and tropical Africa |
| What is Epstein barr virus as a oncogenic virus? | Burkitt's lymphoma, nasopharyngeal carcinoma, B cell lymphoproliferative disease which is found in west Africa, Papua new Guinea, southern china, Greenland and immunosuppressed and immunodeficient patients |
| What does the Human T cell leukemia virus type 1 and Human immunodeficiency virus and human herpes virus do? | it effects RNA, adult T cell leukemia/lymphoma (Kaposi's sarcoma) it is usually found in Japan, the West Indies, and Central Africa |
| What is immune surveillance? | the presumed ability of the immune system to recognize cancer cells at an early stage and eliminate them before they cause disease |
| what are tumor specific antigens? | they are present on tumor cells but not on normal cells and have structures not present in any normal cells |
| what can tumor specific antigens be derived from? | viral proteins, mutant cellular proteins, mutant cellular proteins and amino acid sequences spanning tumor specific recombination sites between genes |
| What are tumor associated antigens | antigens expressed on tumor cells that are also expressed on normal cells in small amounts |
| what do many tumor associated antigens correspond to? | proteins expressed by immature sperm in the testis or by trophoblasts, they don't express HLA-A, B, or class II |
| how can the immune system destroy maliginant tumors? | cancer cells have an excess amount of MIC which is the ligands for the activation of NKG2D, this receptor is on the NK lambda delta and cytotoxic CD8T cells which attack and kill tumor cells |
| What is tumor evasion: MHC class I down regulation? | Down modulation of MHC class I expression will allow tumors to evade detection by CTLs, specific for tumor antigens. Moreover, these tumor cells will have a survival advantage. |
| What is Tumor evasion: NK cell inhibition? | Inhibition of NK cells can by a tumor's ability 2 block recognition of stressinduced top protein MIC expressed on cancer cells. Tumor cells may gain the ability to secrete MIC, soluble form binds 2 NK receptor blocking tumor recognition & destruction |
| What is tumor evasion by suppression? | i. General immune inhibition occurs if tumors develop the ability to secret inhibitory cytokines, such as TGF-beta or IL-10. Many cancerous tumors are found to be associated with T-reg cells that block the activation of tumor infiltrating T cells. |
| What is tumor evasion by the tumor load? | this where the immune system may go unnoticed by the immune system and it grows too large before the immune system notices it and by that time it is too big for the immune system to fight |
| Cytokines | regulate the intensity, duration and characteristics of immune responses act on target cells by binding to receptors are proteins secreted by activated leukocytes |
| Which of the following statements about inflammation is false? | Since inflammation is an immune response, it will not cause harm to self tissues. |
| Which of the following is not considered to be a component or characteristic of adaptive immunity? | first line of defense |
| Gene rearrangements events | occur in developing B cells |
| Which of the following statements about neutrophils is false? | They process and present antigens to T cells. |
| Numerous vaccination procedures require multiple booster shots because | repeated exposure to an antigen builds up a larger pool of antigen specific memory cells. |
| Which of the following statements about TLRs is true? | They are pathogen recognition receptors (PRRs). |
| Which of the following statements regarding CD8 T cells is incorrect? | CD8 binds to the peptide binding domain of MHC and thus contributes to antigenic specificity of CTLs |
| Which of the following is not considered to be a component or characteristic of innate immunity? | Antigen specific activation and memory. |
| Which of the following statements is true? | Opportunistic pathogens cause disease in individuals with weak or impaired immune systems. |
| Immunoglobulin gene rearrangement during B cell development results in | assembly of a complete antibody coding sequence that is suitable for expression. and diversity of antibody specificities. |
| The T-cell co-receptor CD4 interacts with _______ bound to the surface of _______: | MHC class II; APCs |
| Which of the following is not considered to be an antibody effector function? | Cell-cell communication |
| Which of the following characteristics is common to both T-cell receptors and immunoglobulins? | Somatic recombination of V, D and J segments results in tremendous diversity of antigen-binding sites |
| Which of the following corresponds to an immunoglobulin antigen binding site? | the pairing of light and heavy chain V regions |
| Which of the following is associated with antigen presentation by MHC class I? | Antigens are derived from proteins translated in the cytosol of the presenting cell. |
| Humanization of monoclonal antibodies is done in order to | avoid a HAMA response. and create antibodies suitable for clinical treatment of human diseases. |
| Which of the following describes the sequence of events involved in processing of peptides that will be presented as antigen with MHC class II? | endocytosis lysosomal protease activity removal of CLIP from MHC class II binding of peptide to MHC class II peptides presented on plasma membrane |
| Which of the following isotypes is not associated with a clear effector function? | IgD |
| Which of the following does not apply to MHC class II molecules? | HLA-A, HLA-B, HLA-C |
| An allergic reaction to poison ivy is associated with _____. | CTL activation |
| An example of type III hypersensitivity is _____. | serum sickness |
| Which one of the following types of immune responses is least beneficial in clearing helminth infections in the intestinal tract? | Th1 cytokines |
| The accumulation of variant HIV viruses that evade detection by memory B cells and T cells, and that develop resistance to drug regimes are attributed to | error prone reverse transcriptase |
| During the course of a successful desensitization process, the patient’s antibodies will change from an _____isotype to an _____ isotype. | IgE:IgG |
| Which of the following statements about M cells is false? | They process and present antigens directly to T cells. |
| Which description of HAART is false? | it cures aids |
| Most common over-the-counter NSAIDs | block prostaglandin synthesis |
| Systemic anaphylaxis is typically triggered by the presence of allergen in _____. (this came from answer key) | the circulation |
| _________ migrate to secondary lymphoid tissues, whereas ____________ migrate to inflamed tissues. | Central memory T cells; effector memory T cells |
| ___________ is a virus associated with development of cervical cancer. | human papillomavirus (HPV) |
| human herpes virus 8 (HHV8) | Kaposi's sarcoma |
| Which of the following is not considered to be a mechanism by which tumors can evade immune detection? | enhancement of inflammatory responses |
| When an individual receives a kidney transplant, the concern will be to control the development of _____. | allorecognition type I hypersensitivity reactions |
| Cancers develop their own blood supply and become vascularized through a process called _____. | angiogenesis |
| Chemical and physical agents that increase mutation rates by damaging DNA and increase the likelihood of developing cancer are known as _____. | carcinogens |
| Systemic distribution of cancer cells to other sites of the body through the bloodstream or lymph is a process known as _____. | metastasis |
| Which of the following is not considered to be an example of cancer immunotherapy? | radiation treatment |
| Which of the following is likely to be accepted? | syngeneic graft |
| What is a xenograft? | transplants between species- are the LEAST likely |
| Which of the following pairs of terms do not belong together? | pro-B cell / somatic hypermutation |
| with a deficiency in the AIRE protein suffer from a broad spectrum autoimmune disease that involves immune attack against a diverse set of body tissues and organs. Which statement below most accurately provides a mechanistic explanation of this disease? | These patients suffer from a defect in negative selection of thymocytes |
| Which of following events does not occur in the bone marrow? | rearrangement of TCR genes. |
| When a T cell binds to Ag/MHC presented by an APC that does not express B7, | the T cell becomes anergic |
| Which of the following is true about both T cell and B cell activation signaling pathways? | They both involve phosphorylation of ITAMs on the cytoplasmic tails of plasma membrane proteins. They both involve cleavage of membrane phospholipids called PIP2. They both involve the RAS/MAPK pathway. |
| In MHC molecules, most variation in amino acids occurs | in the antigenic peptide binding groove |
| The activation of naïve CD8 T cells to become effector CTLs: | requires binding to B7 on dendritic cells is aided significantly by CD4 T cell secretion of IL-2 requires specific recognition of peptide antigen in MHC class I |
| Hematopoietic stem cells | are self-renewing cells that give rise to all blood cell types |
| Which of the following is false regarding the function of the surrogate light chain? | Serves as a co-receptor in mature B cells |
| Which of the following does not apply to the thymus gland? | Th2 differentiation |
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