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Immunology Exam 1
| Question | Answer |
|---|---|
| What is the origin of immunology? | clinical observation that survivors of epidemics were resistant to subsequent re-infection. |
| what is vaccination? | prior exposure to a pathogen in avirulent form to induce immunity. |
| why does infection occur despite immune system? | Immune system requires time to mount maximally effective response. It adapts so that it has a more rapid response on the second exposure. |
| how were most vaccines produced? | by trial and error. mechanism of immunity is not necessarily understood. its difficult to produce new vaccines. |
| what is the main purpose of the immune system? | to protect against infectious diseases. |
| commensal species? | many microorganisms live together, such as inside the healthy gut. |
| flora? | community of microbes at given anatomical site. |
| what is a pathogen? | infectious organism that causes disease. |
| opportunistic pathogens? | cause illness only when bodys defenses weakened or they reach an unusual anatomic site. |
| how can infection be controlled? | eliminating pathogen of by limiting the size and location of population. |
| how does a pathogen change over evolutionary time? | adapts to replicate and be transmitter; disease in host can be maladaptive. |
| what is the first line of defense against infection? | skin. barrier (keratinized apithelium) breached by physical damage. |
| what type of defense is mucous? | physical and chemical defense that occurs in the respiratory, gastrointestinal, urogenital epithelia. |
| what antimicrobial substances are secreted by epithelia? | sebum, defensins, tears, saliva, acid pH. |
| what does the innate immune response cause at the site of infection? | inflammation. |
| what immune response is responsible for eliminating pathogens that breached surfaces? | innate immune response. |
| How does the innate immune response react quickly? | recognition by soluble proteins and cell-surface receptors of pathogen, its products, or altered host cells/proteins. Recruitment of effector mechanisms to destroy pathogen. |
| how is the innate immune system determined? | by the genes inherited from parents. |
| what is the function of cytokines? | produced by cellls and proteins sensing presence of pathogen trigger the innate immune response. |
| what is the function of capillary dilation as a response to infection? | increases blood flow - redness, warmth. |
| adaptive immune response? | highly specialized for the pathogen. |
| how are innate and adaptive immunity different? | pathogen recognition receptors differ, effector mechanisms similar. |
| What is one reason pathogenic microorganisms have an advantage in the host they infect? | They reproduce and evolve more rapidly than the host can eliminate them. |
| What is associated with mucosal surfaces? | Mucus-secreting goblet cells. Lysozyme, M cells, beating cilia. White pulp is NOT associated with mucosal surfaces. |
| What is characteristic of inflammation? | pain, increased vascular permeability and edema, vasodilation, influx of leukocytes. |
| What is the basic function of eosinophils? | defense against parasites. |
| what is the basic function of natural killer cells? | kills virus infected cells. (also cancer) |
| What is the basic function of erythrocytes? | oxygen transport. |
| what is the basic function of macrophages? | phagocytosis and killing of microorganisms. |
| what are examples of granulocytes? | neutrophils, basophils, eosinophils. Monocytes are NOT granulocytes. |
| Waht is the most abundant type of leukocyte in the human peripheral blood? | neutrophils. |
| B cells differentiate into? | plasma cells |
| what do megakaryocytes produce? | platelets. (thrombocytes) |
| What do myeloid progenitor cells produce? | neutrophils, macrophages, basophils, eosinophils. |
| What do hematopoetic stem cells give rise to? | white blood cells and red blood cells.(all blood cells really) |
| what do platelets participate in? | clotting reactions to prevent blood loss. |
| During human development, where does hematopoiesis take place? | different anatomical locations. |
| Where do megakaryocytes reside? Under what conditions do they travel? | They do not circulate and reside only in the bone marrow. |
| How are new hematopoietic stem cells created? | Hematopoietic stem cells are self-renewing |
| describe the flow of lymph through a lymph node draining an infected tissue | afferent lymphatic vessel to lymph node to efferent lymphatic vessel. |
| Waht is the predominant route by which pathogens are brought from a site of infection into the lymph node? | afferent lymphatics. |
| Describe complement components. Location, function, activation? | soluble proteins, located in extracellular spaces, some function as proteases once activated, activated by a cascade of enzymatic reactions. |
| Waht is the membrane-bound form of C3 convertase of the alternative pathway of complement activation? | C3bBb |
| Waht are the plasma proteins that counteract the activity of factor P by activating C3 convertase through the cleavage of C3b? | Factor H and Factor I |
| Waht polymerizes to form a transmembrane channel that compromises the integrity of cell membranes? | C9 |
| Waht is the ligand for CR3 and CR4 formed by the cleavage of C3b by the combined actions of factors H and I? | iC3b |
| What are the actions of the coagulation system? | blood clot formation, decrease in blood loss and fluid through interstitial spaces in tissues. Release of inflammatory mediators by platelets, and wound healing. |
| Waht is characteristic of C-reactive protein? | acts as an opsonin by binding to phosphocholine of pathogens, induced by elevated IL-6, a member of the pentraxin family, triggers the classical pathway of complement activation. NOT sythesized by the spleen. |
| Waht TLR3 and TLR4 adaptor proteins participates in the activation pathway that culminates in the synthesis of type I interferons? | TRIF and TRAM. |
| Waht is characteristic of septic shock? | organ failure, high mortality rate, compromised blood supply vital to organs, disseminated intravascular coagulation. NOT blood vessel constriction. |
| What is an endogenous pyrogen? | cytokines made by the host that increase body temperature. |
| Which chains need only VJ rearrangement? Which need VDJ rearrangement? | VJ: Immunoglobulin light chain, T-Cell receptor alpha chain. VDJ: Immunoglobulin Heavy chain, T-cell receptor Beta chain. |
| In most cases, what does the adaptive immune response rely on the initial activation of in secondary lymphoid tissue? | t cells |
| What is characteristic of native antigen recognized by t cells? | peptides ranging between 8 - 25 AA in length. AA sequences not found in host proteins. Primary, not secondary, structure of protein. Binding to MHC on the surface of antigen-presenting cells. NOT requiring degradtion for recognition. |
| Describe CD8 tcells. | CD8 is also known as CD8 T-cell co-receptor, binds to MHC molecules @ site distinct from that bound by the t-cell receptor, kills pathogen infected cells by inducing apoptosis, are MHC class I-restriced. DOES NOTactivate b cells. |
| What characteristic permits activated CD8 Tcells to destroy and cell type harboring viable and replication pathogens such as viruses? | MHC class I molecules are expressed ubiquitously by most neucleated cells. |
| How do the 5 isotypes of immunoglobulin differ from each other? | Differ in their heavy chain constant regions/ |
| Waht does a circulating B cell that has never before encountered an antigen express on the cell surface? | IgM and IgD |
| Which antibody is transported across mucosal epithelia? | IgA |
| What is the mutation mechanism that results int eh production of antibodies that bind antigen with higher affinity called? | somatic hypermutation |
| Waht is the process that results in change int he constant region of the heavy chain of antibodies, causing a change in the effector function and transport properties of antibodies? | Isotype switching. |
| What characteristics describe B-cell receptors? | Are membrane bound and secreted, consist of variable region and constant region, possess specificity and can therefore bind only to unique epitopes, undergoes affinity maturation as a consequence of somatic hypermutation. |
| What is the antigen-binding site of an immunoglobulin formed from? | paired V regions of a single heavy chain and a single light chain. |
| What contributes to antigen specificity of immunoglobulin, and what makes up the more conservative flanking regions? | Hypervariable loops; framework regions. |
| What is somatic hypermutation? | the rearrangement of V, D, and J segments to form an immunoglobulin. neucleotide changes in variable regions of immunoglobulin genes affecting affinity for antigen. |
| What is isotype switching? | change of immunoglobulin class but preservation of antigen specificity |
| What does V(D)J recombinase do? | it is the enzyme responsible for recombining V, D, J segments during somatic recombination. |
| What is the main function of IgE? | to mediate sensitization of mast cells and defense against parasites. |
| What is associated with activation-induced cytokine deaminase (AID) activity? | Synthesized in proliferating B cells during active immune responses, somatic hypermutation, isotype switching, cytosine conversion to uracil. NOT diversification of the V<sub>H</sub> domain but not the V<sub>L</sub> domain. |
| What characeristic is common in both T-cell receptors and immunoglobulins? | Somatic recombination of V,D,J segments is responsible for the diversity of antigen-binding sites. |
| The antigen-recognition site of T-cell receptors is formed by the association of which of the following domains? | Valpha and Vbeta. |
| In terms of V, D and J segment arrangement, the T-cell receptor <alpha>-chain locus resembles the immunoglobulin _______ locus, while the T-cell receptor <beta>-chain locus resembles the immunoglobulin _______ locus: | C. kappa light chain; heavy chain |
| In B cells, transport of immunoglobulin to the membrane is dependent on association with two invariant proteins, Ig<alpha> and Ig<beta>. Which of the following invariant proteins provide this function for the T-cell receptor in T cells? | CD3gamma , CD3delta, CD3epsilon, zeta. (all of the above is the multiple choice answer.) |
| MHC class II molecules are made up of two chains called _______, whose function is to bind peptides and present them to _______ T cells: | alpha and beta; CD4 |
| The peptide-binding groove of MHC class I molecules is composed of the following extracellular domains: | alpha1:alpha2 |
| What is the sequence of events involved in processing of peptides that will be presented as antigen with MHC class I? | proteasome -- TAP1/2 -- endoplasmic reticulum --MHC class I -- plasma membrane |
| What is the sequence of events involved in the processing of peptides that will be presented as antigen with MHC class II? | endocytosis -- protease activity -- removal of CLIP from MHC class II -- binding of peptide to MHC class II -- plasma membrane. |
| The complementarity-determining region (CDR) 1 and CDR2 loops of the T-cell receptor contact the _______ | alpha helices fo the MHC molecule. |
| The high degree of polymorphism in MHC class I molecules that present antigens to CD8 T cells is found in _______ because _______ is/are monomorphic: | D. the heavy chain; beta2-microglobulin |
| What cell-surface markers differentiates hematopoietic stem cells from other cell constituents in the bone marrow? | CD34 |
| What is characteristic of a large pre-B cell? | VDJ is successfully rearranged and <mu> heavy chain is made |
| In what order do light-chain genes rearrange? | The kappa light-chain genes rearrange before the lambda light-chain genes. |
| Stromal cells produce _______, which is a secreted B-cell development growth factor influencing the progression of B cells from the late pro-B-cell to the pre-B-cell stage: | IL-7 |
| what happens to Developing B cells that fail to make productive D to J heavy-chain rearrangements on both homologous chromosomes | die by apoptosis in the bone marrow. |
| Pro-B cells produce a surrogate light chain, which associates with the <μ> chain on the cell surface. The surrogate light chain is composed of what? | VpreB and lambda5 |
| What is An important advantage of having two gene loci (<kappa> and <lambda>) for the light chain? | that the likelihood of a successful rearrangement of light-chain genes increases. |
| A defect in what protein blocks B-cell development at the pre-B-cell stage, resulting in almost no circulating antibodies in individuals with this defect? | Btk. (Brunton's tyrosine kinase) |
| What characterizes the B-1 cells that develop prenatally? | They lack N nucleuotides. They possess poly specificity for bacterial polysaccharide antigens. They arise early in embryonic development preceding the deveolpment of the majority subset of B cells and theyhave little or no IgD on the cell surface. |
| Receptor editing involves what? | successive rearrangement at the light-chain loci when reactivity to self antigen occurs during B-cell development. |
| What are the four classes of pathogen the provoke immune responses? | Bacteria, viruses, fungi, and parasites. |
| What is a bacterium that causes a common disease in a population that has been previously exposed to it called? | Endemic. |
| What are the epithelia in the human body that act as barriers to infection? | Skin, gastrointestinal tract, respiratory tract, urogenital tract. |
| What are the main ways in which epithelia carry out their barrier function? what mechanisms are employed? | Mechanitcal barriers: tight junctions.Flow of air over surfaces preventing anaerobes. mucous movement from cilia(respiratory) Chemical:fatty acid sebaceous glands, lysozyme, acid(stomach), pepsin, defensins. Microbial barriers: nonpathogenic flora. |
| What is a defensin? | an antimicrobial peptide that protects epithelial surfaces from pathogens. |
| How can antibiotics upset the barrier function of intestinal epithelia? What is a specific example of this? | Antibiotics attack microbiological barriers of intestinal epithelia. |
| What are the characteristics commonly associated with inflmamation and what causes them? | Heat, redness, pain, swelling(edema). Caused by vasodilation, increased vascular permeability and consequent infiltration of fluid and leukocytes from blood of infected site. |
| What is characteristic of innate immunity? | inflammation, fast response, cytokine production. |
| What is characteristic of neutrophils? | active only in aerobic conditions. |
| What are the main differences between innate immunity and adaptive immunity? | Innate: initiated almost immediately. General recognition mechanisms. Unable to eradicate pathogen completely usually. Adaptive: specific recognition, eradicates pathogen, provides long term protective immunity through memory. |
| What are the 2 main progenitor subsets of leukocytes? Where do they originate in adults? | lymphoid progenitor and myeloid progenitor. In adults all leukocytes originate from bone marrow and are derived from pluripotent hematopoietic stemcells. |
| What white blood cells differentiate from Lymphoid and myeloid progenitors? | Lymphoid progenitor: B cells, T cell, NK cell. Myeloid progenitor: basophils, eosinophils, neutrophils,mast cells, dendritic cells, and monocytes. |
| Primary lymphoid tissues are the sites where lymphocytes _______, whereas secondary lymphoid tissues are the sites where lymphocytes _______. | develope and mature; become stimulated |
| How does the spleen differ from the other secondary lymphoin organs? | spleen has no connection with lymphatics. |
| what is colonal selection and colonal expansion in the context of an adaptive immune response? | Selection: only those lymphocytes that can recognize particular pathogen and respond are selected to participate in immune response. Expansion: proliferation and subsequent differentiation of these few lymphocytes to provide large numbers of effector cel |
| waht would be the consequence of a bioterrorist attack that released small pox into a city? | Last case of small pox was 1970s thus large portion of population is susceptible. ~30-50% mortality rate. |
| MATCHING: which is mismatched? a. cytosol: intracellular pathogen b. surface of epithelium: extracellular pathogen C. Nucleus: intracellular pathogen d. Lymph: intracellular pathogen | D. Lymph: intracellular pathogen.Lymph nodes perform three functions:filter lymph, preventing spread of microorganisms +toxins that enter interstitial fluids. destroy bacteria/toxins/particulates by phagocytic action of macrophages. produce antibodies. |
| Describe the enzymatic reaction known as complement fixation | cleavage of C3 into C3a and C3b and the covalent bonding of C3b to pathogen surface is called complement fixation. All pathways converge. |
| what enzyme is responsible for the compliment fixation reaction in the alternative pathway? | C3 convertase. It differes in composition depending on which pathway. LEctin and classical use C4b2a whereas alternative uses C3bBb |
| What three effector mechanisms of complement are enabled by the complement fixation pathway? | C3b binds and tags pathogens for phagocytosis thru binding to receptor CR1. C3b contributes to C5 convertase, catalyses assembly of terminal complement components and membrane atk complex. C3a is inflammatory mediator recruits inflammatory cells to site. |
| What is not a soluble form of C3 convertase of the alternative pathway of complement activation? | IC3bB |
| What are the steps that take place when a bacteria is opsonized via C3b:CR1 interaction between the bacterium and resident macrophages in tissues? | CR1 on macrophage binds to C3b coating bacteria. Macrophage then engulf bacterium. Forms phagosome then fuses with lysozome to form phagolysosome where toxic mediators and degradative enzymes are localized. bacteria destroyed. |
| What are the (1) soluble and (2) cell surface-associated complement control proteins that operate in the terminal stages of the alternative pathway of complement activation? What are their activities? | Soluble: S protein, clusterin, and factor J which all inhibit C5b,C6 and C7. Surface associated proteins: homologous restriction factor(HRF) and CD59(protectin) which both prevent C9 recruitment and thus C9 polymerization. |
| What are the differences between the 3 pathways of complement in terms of how they are activated? (lectin, alternative, classical) | Classical: 2 ways of activation;antibody bound to pathogen, or presense of C reactive protein. Lectin: requires mannose binding lectin. Alternative: requires an activating surface of pathogen, which stabalizes complement components. |
| What is the ligand(s) to the lectin receptor? | Carbohydrates (e.g., mannose and glucan) |
| What is the ligand(s) to the scavenger receptor? | Negatively charged ligands (e.g., sulfated polysacchardise and neucleic acids) |
| What is the ligand(s) to CR3? | IC3b, lipophosphoglycan, filamentous hemagglutinin, lippopolysaccharide (LPS) |
| What is the ligand(s) to CR4? | IC3b, lipophosphoglycan, filamentous hemagglutinin, lippopolysaccharide (LPS) |
| What is the ligand(s) to CR1? | C3b |
| What is the ligand(s) to TLR4:TLR4? | LPS/lippopolysaccharide |
| What is the ligand(s) to TLR5? | flagellin |
| What is the ligand(s) to TLR3? | RNA |
| Other than ligand specificity, what is a key difference between TLR5, TLR4, TLR1:TLR2, and TLR2:TLR6 compared to TLRs 3,7,8, and 9? | TLR5, TLR4, TLR1:TLR2, and TLR2:TLR6: transmembrane receptors anchored on plasma membrane interacting with extracellular locations. TLRs 3,7,8, and 9: anchored in endosomal membranes located in cytosol = intracellular. |
| Why can TLRs detect many different species of microbes despite the limited # of different TLR proteins? | because many pathogens possess features that are common to different groups of pathogens(LPS in gram negative bacteria) |
| What is the importance of NFκB in mediating signals through TLRs? | NFκB is a transcripition factor found in cytoplasm in inactive form in macrophages before activation. Signaling results in phosphorylation cascade that converts NFκB to active form allowing transcription of genes enabling effector capacity of macrophage. |
| What is the name given to the earliest intracellular vesicle that contains material opsonized by macrophages? | phagosome |
| What are the main similarities/differences in the general properties and roles of macrophages and neutrophils? | both phagocytic produced by bone marrow, produce defensins. Macrophages are resident in tissue, neutrophils circulate in blood. Macrophages are long lived and act in recruitment of neutrophils to infected tissue. Macrophage carry Toll-like receptors(TLR4) |
| How do both macrophages and neutrophils destroy pathogens? | Ingest microorgansims by phagocytosis. takes to phagolysosome. Destroyed by bactericidal substances. |
| What does vascular endothelium produce in responce to TNF-<alpha> that induces localized blood clotting? | platelet activating factor. |
| What induces the production of type 1 interferon by virus-infected cells? | Type 1 interferon genes (encoding interferon alpha and beta are transcribed as a result of the presence of double stranded RNA. |
| Do normal cells produce double stranded RNA? Why/why not? | normal cells do not contain double stranded RNA |
| What are the mechanisms by which type1 interferons exert their antiviral effects? | Type 1 interferons block virus replication in infected cells and protect uninfected cells frm becoming infected. Induce cellular genes that destroy viral RNA and inhibit viral RNA synthesis. Also activates NK cells. |
| What activities are most closely associated with natural killer cells? | lysis of virus infected cells. |
| Why is factor I deficiency associated with infections caused by pyogenic bacteria? | rapid turnover and consumption of C3 in serum causes inefficient fixation of C3b on surface of pathogens, compromising opsonization and phagocytosis. |
| What is the most likely protein defect to cause an inability to generate reactive oxygen intermediates during respiratory burst in phagocytes? | NADPH oxidase subunit. |
| What are advantageous features that distinguish vertebrate adaptive immune responses from the innate immune responses made by both vertebrates and invertebrates? | unique differences distinguishing particular pathogens from other pathogens and from vertebrate host are targeted specificaly. |
| What is clonal selection? | the process by which a pathogen stimulates only those lymphocytes with receptors specific for that pathogen. |
| Why is a pathogen most capable of causing disease the first time it is encountered? | it takes several days for immune system to generate adequate numbers of pathogen-specific lymphocytes after clonal selection. |
| What is characteristic of b-cell and t-cell receptors? | Antibodies are secreated form of Bcell receptor whereas immunoglobulins are transmembrane. Diversity generated by same molecular process. both receptors are expressed as transmembrane polypeptides. T more restrictive than B in range of antigens they bind |
| What is somatic recombination? | It is the process that results in the recombination of gene segments of the tcell receptor and immunoglobulin genes giving rise to lymphocytes with unique specificities for antigens. |
| In a typical infection, dendritic cells first encounter pathogen in _______, and then transport it to _______ where pathogen-derived peptide fragments are presented to _______. | infected peripheral tissue; secondary lymphoid tissue; t-cells. |
| What are the fundamental differences between CD4 and CD8 T cells in terms of their effector function and their interation with MHC molecules? | CD4 T cells: secrete cytokines that instruct other cells to acquire effector function. CD8: differentiates into cytotoxic effector cells and kill target cells. |
| What are the major sources of pathogen derived antigens recognized by T cells? | CD8: antigen in intracellular sites in host (usually viruses but some bacteria that live in cells) CD4: antigen from extracellular fluid and interstitial spaces between cells. |
| Why is it advantageous to the host to use different effector mechanisms to combat antigens encountered in both intracellular and extracellular sites. | Host immune response must identify all types of pathogen in various locations. |
| How does MHC class I molecules encounter the peptides to which it binds and ultimately presents to T cells? | does not bind to peptides derived from pathogen-derived proteins until peptides transported to ER lumen. peptide:MHC class I complex goes to surface to present to CD8cells. |
| How does MHC class II molecules encounter the peptides to which it binds and ultimately presents to T cells? | bind peptides in endocytic vessicles. presents to CD4 t cells. |
| What is the main function of IgG? | IgG is the main antibody isotype found in blood and extracellular fluid allowing it to control infection of body tissues |
| What is the main function of IgA? | plays a critical role in mucosal immunity. secretory component of IgA protects from being degraded by proteolytic enzymes, thus IgA can survive in harsh gastrointestinal tract environment+protect against microbes that multiply in body secretions |
| What is main function of IgD? | found in very small amounts in blood. In B-cells, functions to signal B-cell to activate. coexpressed with IgM. |
| What is the main function of IgM? | Complement activation, causes C3b to bind to the antigen. It is the first antibody to appear in response to initial exposure to antigen. |
| Why would a vaccine based solely on carbohydrate moieties (capsular polysaccharides) be ill conceived if the goal was to stimulate antibody responses as well as strong helper T-cell response? | for CD4 T helper cells to participate in B cell activation, protein sequences must be included in the vaccine. |
| What are the similarities and differences between neutralization and opsonization? | Similar in that once antibody is bound to antigen it is targeted for destruction by phagocytes after ingestion. They differ in thatneutralization in binding to antigen, the host cell is unable to bind native anitgen, uptake blocked, antigen inhibited |
| If there are no receptors on macrophages for the constant region of IgM, how does IgM coating a pathogen promote its phagocytosis? | IgM induces classical pathway. leading to the deposition of C3b on the pathogens surface. Phagocytes contain complement receptor CR1 which binds to C3b. opsinization ensues. |
| What are the two mutational mechanisms that drive the enhancement of antibody quality in activated B cells? | somatic hypermutation and isotype switching. |
| What are the types of unwanted and potentially harmful immune responses? | Allergies and autoimmune diseases. Transplant rejection. |
| What's the difference between antibodies and immunoglobulins? | immunoglobulins are membrane bound. antibodies secreated. |
| Which type of cell produces antibodies? which type of cell produces immunoglobulins? | Immature, mature and memory B cells have immunoglobulin. Plasma cells produce antibodies. |
| Describe the structure of an antibody molecule and how this structure enables it to bind to a specific antigen. | 4 polypeptide chains. 2 identical heavy chains + 2 identical light chains. Disulfide bonds hold it together. |
| What are antigens? | the molecules to which antibodies bind. |
| What is an epitope? | specific part of antigen that is recognized by an antibody. |
| What does multivalent antigen mean? | complex macromolecules that contain more than one epitope. |
| how do linear epitopes and conformational epitopes differ? | epitopes in proteins that comprise a contiguous sequence. conformational epitope is formed by AAs brought together by protein folding. not adjacent. |
| how do antibodies bind their antigens? | noncovalent bonding. H-bonds, hydrophobic interactions, van der waals. |
| What is the final arrangement of gene segments in the rearranged immunoglobulin heavy-chain gene V region, and in what order do these gene segment rearrangements occur? | A D gene segment first joins to a J to form DJ, followed by a V becoming joined to DJ to form VDJ |
| In what order do the various immunoglobulin gene loci rearrange? | heavy chains before light chain. Light chain kappa locus before the lambda locus. |
| From what does junctional diversity during gene rearrangement result? | P and N neucleotides. |
| What would be the effect of a genetic defect that resulted in a lack of somatic recombination between V,D,and J segments? | an individual with a genetic defect would be unable to rearrange either immunoglobulin or T-cell receptor genes somatically. =SCID. |
| What is characteristic of the production and use of monoclonal antibodies? | Monoclonal antibodies have specificity for only 1 epitope. Formed by Bcells fused with a tumor cell called a myeloma, to immortilize the resulting hybridoma. Antibodies made in mice have limited therapeutic potential but Humanized ABs reduse complications |
| What is alternative RNA processing? | the process used to produce either surface or secreted forms of the immunoglobulin heavy chain. |
| What are the ways in which T-cell receptors are similar to immunoglobulins and in what ways are they different? | Similar: Receptor has a similar overall structure to membrane-bound Fab frag. of immunoglobulin containing antigen-binding site, 2variable domains + 2constant regions.Both generated thru recombination. |
| Compare the organization of Tcell receptor<alpha> and <beta> genes with the organization of immunoglobulin heavy-chain and light-chain genes. | both contain V and J segments with no D segments. |
| why dont tcell receptors undergo isotype switching? | are not made in secreted form and do not contribute to T-cell effector function. other molecules secreted by T-cells are used for effector functions. |
| What is the role of CD3 proteins and <zeta>(ζ) chain on the surface of the cell? | Transduce signals to the interior of the cell. |
| What do CD8 T cells do when they make contact with virus-infected cells? | kills the virus infected cell/ |
| What do CD4 T cells do when they make contact with macrophages? | They enhance microbicidal powers of macrophages. |
| What do CD4 T cells do when they make contact with B cells? | stimulate B cells to differentiate plasma cells to divide. |
| What is the immunological consequence of SCID caused by either a genetic defect in the RAG-1 or RAG-2 gene? | a lack of somatic recombination in T-cell receptor and immunoglobulin gene loci. |
| Describe the MHC class 1 molecule identifying the different poly peptide chains and domains. | heterodimer made of one ,alpha> chain and a smaller beta2-microglobulin. Alpha chain consists of 3 extracellular domains and a transmembrane region and a cytoplasmic tail. |
| What are the names of the MHC class 1 molecules produced by humans? which part of the molecule is encoded within the MHC region of the genome? | HLA-A, HLA-B, and HLA-C. |
| Describe the MHC class 2 molecule identifying the different poly peptide chains and domains. | Alpha an beta chain heterodimer. Alpha chain consists of a1 and a2 extracellular domains, a transmembrane region, and a ctyoplasmic tail. Beta chain consists of B1 and B2 extracellular domains, transmembrane region and cytoplasmic tail. |
| What are the names of the MHC class 2 molecules produced by humans? which part of the molecule is encoded within the MHC region of the genome? | HLA-DP, HLA-DQ, HLA-DR |
| Which domains/parts of MHC class 2 participate in antigen binding, t-cell receptor binding, and t-cell co-receptor binding? | binds in the peptide-binding groove formed by a1 and B1 domains. |
| Where is amino acid variation among MHC class II allotypes the present antigens to CD4 T cells concentrated? | Where the MHC molecule contacts peptide and T-cell receptor. |
| What is antigen processing? | Intracellular breakdown of pathogen-derived proteins into peptide fragments that are of the appropriate size and specificty required to bind to MHC molecules. |
| What is antigen presentation? | Assembly of peptides with MHC molecules and the display of these complexes on the surface of the antigen-presenting cells. |
| Why are antigen processing and presentation required before t cells are activated? | T-cell receptors cannot bind to intact protein, only to peptides and T-cell receptors do not bind anitgen directly but MHC+peptide. |
| What is the order of steps involved in the endogenous antigen-processing pathway for intecellular, cystolic pathogens? | Pathogen proteins in cytosol broken down in proteosomes. Transported to lumen of ER using TAP. Correct motif bind to MHC1. Golgi transports to cell surface. |
| What removes CLIP from MHC class II molecules? | HLA-DM |
| What are the steps involved in the antigen-processing pathway for extracellular pathogens? | Pathogens taken up by endocytosis/phagocytosis and degraded into peptide fragments. Peptide loaded into MHC2 antigen-binding groove. Clip removed. peptide-MHC complex moves to cell surface. |
| What evidence supports the proposal that MHC diversity evolved by natural selection caused by infectious pathogens rather than exclusively by random DNA mutations? | MHC polymorphisms are non-randomly localized predominately in the region of the molecule that makes contact with the peptide and t-cell receptors. |
| What is the order of a B cells life history? | Repertoire assembly, negative selection, positive selection, search for infection, find infection, attack infection. |
| What are the stages of B cell development? | Stem cell, early pro-B cell, late pre-B cell, Large pre-B cell, small pre-B cell, immature B cell. |
| What is the importance of bone marrow stroma for B cell development? | Provides neccessary environment for B-cell development by secreating products and adhesion molecules. Cytokines such as IL-7 have important role in later stage development. |
| What are the two main checkpoints of B-cell development in bone marrow? | Checkpoint 1: formation of μ heavy chain complexed with surrogate light chain VpreBλ5, Ig<alpha> and IG<beta>. Checkpoint 2:complete b-cell receptor. μheavy chain, κ +λ light chains, Ig<alpha> + Ig<beta> on surface of B-cell |
| What is the fate of B-cells that produce functional/nonfunctional heavy/light chains? | @ checkpoint1: if V(d)J rearrangement gives rise to functional pre-B-cell receptor its permitted to survive. If nonfuntional, the pro-B-cell undergoes apoptosis. @checkpoint2: functional light chain=functional surface immunoglobulin and survival. |
| What would be the consequence if Terminal deoxyneucleotidyl transferase (TdT) were expressed throughout the whole of small pre-B-cell development? | N neucleotides would be added at the VJ joints of all rearrangement light chain genes resulting in an increase in imunoglobulin diversity. |
| what would occur after the production of a function <mu> chain as a pre-B-cell receptor? | RAG proteins are degraded. Chromatin structure of the heavy-chain locus is reorganized to prevent gene rearrangement. Transcription of RAG1 and RAG2 genes ceases. There is allelic exclusion of a second <mu> chain. |
| What properties distinguish B-1 cells from B-2 cells? | Unlike conventional B-2 cells, B-1 cells express CD5, posses few N neucleotides at VDJ junctions, and have a restricted range of antigen specificities. Produce low affinity IgM and respond mainly to carbs. vs protein epitopes. |
| Should B-1 cells be categorized as participants in innate immune response or as acquired immune response? | B-1 cells are best associated with innate immune responses because of their rapid response to antigen, their limited diversity and their polyspecificity. |
| What is true of centrocytes? | somatic hypermutation has occured. isotype switching is complete. |
| What is the function of negative selection of B cells? | ensures that autoreactive B cells are prohibited from emerging in the body. |
| Immunological tolerance in the b cell repertoire is called _______ tolerance when it develops in the primary lymphoid organs, and _______ tolerance when it is induced outside the bone marrow. | central; periphreal. |
| What is the role of primary lymphoid follicles in eliminating B cells that have antigen receptors specific for soluble self antigen? | To survive, circulating B cells must enter primary follicles where survival signals are delivered by cells in the follicles, including follicular dendritic cells. If they fail to enter they will die w. a half life of about 3days. |
| What features characterize a plasma cell? | Differentiates in medulla of lymph nodes and bone marrow. Dedicates 10-20% of total protein synthesis to antibody production. Produces secreated immunoglobulin instead of membrane bound form. |
| Why is immunological memory important in acquired immunity? | memory enable faster, more efficient recall responses when antigen is encountered subsequently. Allows body to clear pathogens before they cause disease. |
| How is immunoglobulin expressed during a primary immune response different qualitatively and quantitatively from a secondary response? | Primary: mainly IgM, in low conc. (titer) and low affinity. Secondary: IgG isotype because of isotype switching. Higher titer. Higher affinity because of somatic hypermutation. |
| Why do b-cells isolated from a particular b-cell tumor all express the same immunoglobulin? | B-cell tumor comprises cells all from a single cell. No further maturation of that cell =immunoglobulin expressed at cell surface. All clones thus express same immunoglobulin(same heavy+light chains) |
Created by:
Lord Azith