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IMMUNOLOGY
step one
| Question | Answer |
|---|---|
| What kind of lymphatic organ is the lymph node | secondary lymph organ |
| function of lymph node | filtration, storage, proliferation of B&T-cells and antibody production. |
| Differences bet primary and secondary follicles of the lymph node | primary: dense and dormant secondary: pale central germinal centers-active |
| Where in the lymph node are the primary and secondary follicles found | follicle of cortex |
| where are t-cells housed in the lymph node | paracortex |
| describe paracortex region in cell mediated immunity | enlarged |
| described paracotex in DiGeoges's syndrome? | underdeveloped |
| lymph vessel that drain rt. arm and rt. side of head? | rt. lymphatic vessel |
| Lymph vessel that drains all else? | thoracic duct |
| where are T-cells in the spleen? | periarticular lymphatic sheath. (PALS) |
| Where are the B-cells in the spleen? | within the white pulp |
| what is the Thymus known as? | Finishing school for T-Cells. Enter immature and leave mature |
| what is tve selection of T-cells? | signal to divide and establish clones |
| What is -ve selection of T-cells? | signal to undergo apoptosis because of it's potential for autoimmune conditions |
| where in the thymus does tve and -ve selection occur? | corticmedullary |
| what is clonal anergy? | peripheral deletion that occurs to T-cells with too great affinity for self |
| which antigen presenting cell (APC) first react to a foreign antigen? | Macrophages or any committed lymphocyte. |
| How does the macrophage and yet-unidentified cell acitvate THo? | macrophages stimulate THo via IL-12 and yet-unidentified stimulate THo via IL-4 |
| What is the role of the naive THo? | To make a selection; CMI or humoral immunity. |
| To chose CMI, what is the cytokine produced? | Il-12 by THo to activate Th1 of CMI |
| To chose humoral, what is the cytokine produced? | IL-4 by THo to activate Th2 of humoral immunity |
| once activated, what does Th1 do? | Secrete Y-INF and IL-2 to activate macrophage for independent killing. |
| Once activated, what does TH2 do? | Secrete IL-4 and IL-5, IL-2, to stimulate B-cells to plasma cells and lymphocytes |
| what do plasma cells do? | produce large amounts of antibodies.(ab) |
| how does ab mediated immunity work? | defend against foreign antigen by opsonization, neutralization and complement activation |
| what does opsonins do? | coats antigen to facilitate phagocytosis |
| What is the function does neutralization serve? | prevention of adhesion |
| what is the function of the complement system? | opsonize and phagocytize, and lyse infected cells |
| how does CMI mediate an immune attack? | Via the TH1 arm of the immune pathway, resulting in cellular infiltrates like macrophages and abscess formation. |
| how does ab's mediate an immune attack? | Via the TH2 arm of the immune pathway resulting in formation of plasma cells that result in ab prod. and ultimate opsonin, neutralization and complement activation. |
| eg of CMI gone awry? | graft and organ transplantation rejection |
| eg. of Humoral immunity gone awry? | allergies |
| What is major histocompatibility complex (MHC)? | polypeptide located on cell membrane of all nucleated cells which can mediate an immune response. significant in transplantation. |
| how many classes of MHC have been identified? | 2 classes. Class one and class 2 |
| What do you know about MHC class I? | There are 3 MHC class I gene prod, HLA A,B & C, expressed in co-dominant form. consist of 3 a heavy chain and beta 2 microglobulin light chain. |
| function of MHC class 1? | a peptide binding groove between the 2 a heavy chain, serve to present antigen to the TCR of CD8 cells |
| name one cell without MHCI surface protein? | RBC |
| what do you know about MHC classII? | Also co-dominantly expressed on all APC, with 2 alpha and 2 beta components with one extra-cellular one intracellular domain. MHC classII products are HLA DP,DQ,& DR. |
| What is the function of MHC class II | Same as Class one except it presents to the TCR of the CD4 cells. |
| name the types of cells that have both class I andII surface proteins on their cell membrane? | All APC. macrophages, B-cells, langerhan cells and dendritic cells |
| Where in MHC classI does antigen loading occur? | RER |
| Where in MHC class II does antigen loading occur? | acidified endosome |
| describe the CD3 complex | associated with TCR of T-lymphocyte and is involved in signal transduction. |
| When bacteria is processed and loaded in the acidified endosome, what is the next step? | The loaded TCR flags the antigen on the cell membrane awaiting a TCR |
| once CD4's TCR commits and binds with MHC class II of APC, what happens? | the CD4 secretes IL-12 to activate THo |
| Once CD8's TCR commits and binds with MHC classI, what happens? | cell mediated killing |
| how does the co-stimulatory molecules of CMI work? | Co-stimulatory molecule on APC B7 and C-stimulatory molecule on T-lymphocyte interact to mediate CMI |
| what branch of the immune system is the natural killer cell (NK)? | innate |
| name the cell markers of NK cells | CD16 $ CD 56 |
| What is EBV's target? | CD21 of B-cells |
| which cells mediate the immune response to HSV and EBV | T-lymphocytes and NK cells |
| How many parts to Ig structure? | fab and Fc fragments |
| which portion is embedded in the cell? | the carboxyl terminal of the FC fragment |
| describe the part that is flagged by the cell and opposes the carboxyl terminal? | the amino terminal |
| Describe the hinge region | region where the Fab and FC region are held together by disulfide bonds |
| function of varible region of Fab fragment | recognizes antigen |
| where would you find both heave and light chains? | In the Fab fragment held by dissulfe bonds |
| What is the FC fragment made of? | heavy chains consisting of constant regions |
| function of constant region of IgM and IgG? | Fixes complement |
| what is the function of the hypervariable region of heavy & light chanis? | allows for ab to have a vast number of specificities called ideotype |
| whcih is the better complement activator, IgM or IgG? | IgM because it is a pentamer |
| What is the complement system? | A set of interacting proteins released into the blood after production in the liver. |
| what is their function | they serve as zymogens, participating in a cascade of reactions that culminate mediation of inflammation and lysis by MAC complex |
| describe initiation of complement system | Initiated by the classical pathway when 2 molecules of IgG or IgM bind to C1, or the Alternate pathway. |
| Describe initiation of the complement pathway | more primitive of the 2 pathways. initiated by attraction of early factors to surface of microbes. |
| Where does IgG bind to the Ab molecule? | IgG binds to the Fc region by the hinge region |
| function of Random combination of VJ and VDJ genes | for diversity |
| function of random combination of heavy and light chains? | for diversity |
| define somatic diversity | aka affinity mutation. mutation that occurs after antigenic contact. |
| function of somatic diversity? | for diversity and tighter specificity of the epitope |
| what is terminal deoxynucleotidyl transferase Tdt? | inserts bases withour template at the junction of VDJ segments randomly. All to create more diversity |
| which terminal illness is Tdt a marker | Tdt |
| what 2 Ig do mature B-cells express? | IgM and IgD |
| what is isotype switching? | switching from IgG to IgA to IgE |
| who mediates isotype switching? | cytokines and CD40L |
| which other cell produce different isotypes | plasma cells but does not switch only makes the isotype for which it is cloned. |
| name the ab in a primary response | IgM |
| Describe IgM | a monomer in tissue, pentamer in blood, tve on mature B-cell andfixes complement. No placental access |
| name ab in a secondary response? | IgG |
| Describe IgG | most abundant Ig, fixes complement, good opsonin, neutralizes bacteria, and crosses the placental barrier. |
| how does IgA work to fight infection? | found in secretions that line the mucosa, picks up secretory component from epithelial cells before secretion prevents attachment of bacteria to mucosa. |
| function of IgD? | unclear. Found on the surface of mature B-cells and in serum. |
| functions of IgE | mediate immediate immune response, ie type one hypersensitivity and immunity to helmithic infection. |
| how does IgE mediate it's type of immunity? | induces the release of mediators from mast cells, basopils and eosinophils when Ig is stimulated by the exposure to allergens |
| define allotype | immunologic epitope that is different among members of the same species. may be heavy or light chain. Allotype determines compatibility for transplant. |
| define isotype | immunological epitope common to a single class of Ig. ie IgG, IgA. determined by heavy chain. |
| define ideotype | Ig epitope, determined by antigen binding site. |
| define hapten | small, single antigenic determinants, unable to mount an immune response independently but can if coupled with another protein. |
| name ex. of hapten | meds like asa, streptomycin, sulfa, some opiates, like morphine. |
| mneumonic for remembering function of IL-1 and IL-2. | HOT T-bone sTEAK IL-1 -pyrogen, IL-2 - increased T-cells, IL-3 -increased bone marrow , IL-4 - IgE, IL-5 -IgA. |
| function of IL-1 | endogenous pyorogen, stimulates B & T-cells, nuetrophils, fibroblast, & epithelial cells to grow and differntiate or synthethize prod. |
| function of IL-2 | secreted Th cells and stimulates growth of Th and Tc cells. |
| function of IL-3 | similar function of GM-CSF, secreted by activated T-cells. Increase growth and differentiation of BM stem cells. |
| function of IL-4 | secreted by B-cells, enhances class switching from IgG to IgA, and production and activation of eosinophils. |
| function of IL-8 | major chemotactic stimuli for PMN's |
| function of IL-6 | stimulated by Th cells and macrophages. stimulates prod. of acute phase reactants and Ig's |
| function of IL-10 | secreted by Th2, stimulates Th2 while inhibiting Th1. Encourages humoral immunity while inhibiting cellular. |
| function of IL-12 | secreted by B-cells, naive cells and macrophages and activates NK and Th1. CMI |
| function of Y-interferon | secreted by Th1 cells destroys viral infected cells. |
| function of TNF alpha | secreted by macrophages, increases IL-2 receptor synthesis by Th cells and increases B-cell proliferation. chemotactic to PMN's |
| list surface markers of T-helper cell | CD4, TCR, CD3, CD28, CD40 |
| list surface markers of T-cytotoxic cell | CD8, TCR, CD3 |
| cell surface marker for B-cell | IgD, IgM, B7, CD19, CD20, CD21,CD40L, MHCII |
| cell surface protein of macrophages | MHCII, MHCI, CD14, FC, C3b |
| cell surface protein of NK cells | MHCII, CD16, CD56 |
| cell surface markers for all cells x RBC | MHCI |
| function of TCR | antigenic recognition |
| function of CD40L | class switching |
| function of CD3 | signal transduction by TCR |
| function of CD28 | Tcell receptor for co-stimulatory signal with B7 |
| function of CD19 | co-receptor with B21 for signal activation transduction |
| function of CD20 | unknown role in Bcell activation |
| function of CD21 | receptor for complement fragment C3D, CD21, and for EBV |
| function of C3b | opsonin |
| Another opsonin | IgG |
| function of B7 | APC receptor for co-stimulatory molecule B7 |
| function of CD14 | on monocytes, macrophages and PMN's which binds LPS. Receptor of superantigens |
| function of CD16 | opsonization, ADCC |
| function of CD56 | unknown |
| IL-1 & IL-2 are both endogenous pyrogens. why is that good for infection? | creates harsh environment for growth, causes rt. shift of oxy/Hg curve making Hg for O2 making it available for the oxygen burs kill. |
| What is the complement system | system of proteins which interact and break into split products to fight infection, mediates humoral immunity and inflammation. |
| how many limbs are there to the complement system | 2 pathways: classic and alternate |
| how is the classical pathway initiated? | IgG and IgM |
| how is the alternate pathway initiated? | by reaction of the more primitive split products to the manose-lethicin membrane of bacteria's cell membrane |
| function of the complement system | mediate inflammation, opsonization and lysis |
| mneumonic for classic pathway | GM makes classic cars. (IgG & IgG initiates the classic pathway |
| Name the 1st split product to be produced | C1 |
| Where does C1 bind to the Ig to initiate the System? | clsoe to the hinge region in the FC fragment |
| function of c3b | opsonization |
| function of c1, c2, c3, c4 | viral |
| function of c3a, c5a | anaphylaxsis |
| function of c5a | neutrophil chemotaxsis |
| function of c5b - 9 | mac complex |
| why is IgM a more effective activator than IgG | IgM is a pentamer and can bind x5 more than IgM which is a monomer. |
| result of C1 esterase deficiency | overactive complement due to loss of inhibitory enzyme. |
| clinical presentation of c1 esterase defeciency | angioedema |
| clinical presentation of c3 deficiency | severe, recurrent, pyrogenic, sinus and resp infections. |
| clinical presentation of c6 and c8 deficiency | Neisseria bacteremia |
| what is decay accelerating factor? | regulatory protein of complement. |
| role of INF to uninfected cells? | Places all cells in an antiviral state. |
| what antiviral process does INF induce? | it produces a protein that degrades viral RNA, but not host's. |
| how does INF alpha and gamma fight infection? | Increases MHCI and MHCII expression on all cells. |
| how does INF affect NK cells? | activate Nk cells to kill viral infected cells |
| how does INF enhance CMI? | mediates ADCC: ab dependent cell mediated cytotoxicity. |
| what kind of immunity is achieved by HBV, botulinum toxin etc? | artificial, passive |
| what kind of immunity is achieved by DTaP? | artificial, active |
| is passive immunity slow onset with memory? | No! Rapid and short term with no memory. |
| Hiv+ mom gives birth to baby who is sero- at 6 months. What kind of immunity is this an example of? | passive |
| define antigenic variation? | process of varying antigenic proteins to hide from the onslaught of the immune system. |
| describe 2 mechanism for antigenic variation | 1. DNA rearrangement 2. RNA segment resortment |
| an example of RNA segment reasortment | H. influenza |
| Describe salmonella's mechanism of antigenic variation | 2 flagella variants |
| describe the result of Borellia's mechanism of antigenic varaition. | relapsing fever. |
| Describe Neisseia gonorrhea's mechanism of antigenic variation | pilus protein |
| mneumonic for shift and drift | antigenic shift -fast - epidemics.antigenic drift- slow - pandemic. |
| define anergy | Ocurrs to self reactive T-cells in the periphery of the thymus. Undergoes apoptosis. |
| does B-cells undergo anergy? | yes, but tolerence is less complete than with T-cells. |
| When the T-cell emerges from the BM is it mature? | No, it is immature and naieve with CD4 and CD8 cell srface makrers. |
| when is the T-cell matured? | After it has made a commitment to carry either CD$ or CD8 |
| How does a T-cell show committment | A CD4 T-cell with low affinity for class II receptors or CD8 T-cell with low affinity for class I . |
| What if it has high affinity for its own class? | The the cell line experiences - selection. If not, + selection. |
| Explain how PPD works | Activates Th1 to mediate a CMI response to the mycobacteria tuberculosis antigen. |
| Does encapsulated organisms demonstrate antigenic variation? | No. what they do is directly activate macrophages and T-lymphocytes to release mediate an exaggerated inflammatory response leading to septic shock syndrome. |
| Name the receptor on the macrophage that bind with the APC | CD14 |
| What is type II hypersensitivity? | Cy-2-toxic. Classical pathway activated by IgM and IgG, which binds wit ab to start the omplement system. |
| name examples of type II hypersensitivity | autoimmune hemolytic dz, HDNB, Good Pastures,RF, Graves dz, Billous Pemphigoid, MS, & ITP |
| What is type III hypersensitivity? | antigen/ab/complement complex which induces PMN's to the area, that releases its lysosomal enzymes causing tissue distruction. |
| name examples of type III hypersensitivity | PAN, immune complex glomerulonephritis, RA, SLE. |
| describe how serum sickness fits into the category of type III hypersensitivity. | ag/ab complexes, five days post exposure release complement that mediate tissue destruction. |
| clinical presentation of serum sickness | fever, uticaria, arthralgias, proteinemia, lymphadenopathy, 5-10 days post exposure. |
| How is arthrus formation type III hypersensitivity? | via local injection of antigen, where an ag/ab/complement complex forms. |
| example of dz causig arthrus formation | Farmaers lung- hypersensitivity pneumonitis and thermophilic actinomycetes. |
| define type IV hypersensitivity | T-cell mediated. Once sensitized T-cells release lymphokines once antigen is encountered |
| Is the reaction immediate? | No, clinical presentation is delayed and occurs contact with the antigen. |
| In latex allergy, which hypersensitivity is in effect? | Depends on the onset of sysptoms. I immediate-Type I, If delayed-type II. |
| Nmae the 4 T's of type IV hypersensitivity. | T-lymphocytes, Transplant rejection, TB skin test, Touching-contact dermatitis like poison ivy. |
| mnuemonic for hypersensitivity. | Anaphalactic and atrophic -I, cytotoxic, ab mediated - II, immune complex complement -III, Delayed -IV. ACID |
| what is Burton's agammglobinemia? | X-linked recessive, decreased production of B-cells. |
| describe B&T cells combined immune deficiency.SCID | defect-early stem cell differentiation. Recrrent bacterial, fungal,protozoal infection to opportunistic illness. |
| Cause of SCID? | multiple causes but most frequent is adenosine deaminase degiciency. |
| other causes of SCID? | IL-2 receptor impairement and failure to synthesize MHC II antigens |
| What dz presents with disseminated mycobacterial infections? | T-cell IL-2 deficiency. |
| defects on CD40L on T-cells causes what dz? | hyper IgM syndrome with decreased class switching and loss of humoral limb. |
| clinical presentation of hyperIgM. | overactive CMI- pyogenic infections. Elevated serum IgM and decreased IgE, IgG & IgA. |
| what is Wiskott-Aldrich syndrome? | X-inked defect causing an inability to mount an IgM response to capsular polysaccharide of bacteria. |
| How does serum levels of Ig present in wiskott-Aldrich syndrome? | IgE - normal and low IgM |
| Wiskott-Aldrich's presentation | WIPE: with pyogenic infections, purpura(thrombocytopenic), and Eczema |
| What is Job's syndrome? | Failure of INF-gamma production of T-helper cells so PMN's has no chemotactic stimulation |
| how does job's syndrome present | retained primary teeth, recurrent colds, and staph abscess, eczema and coarse features. |
| Serum level in Job's syndrome? | Increased levels of IgE |
| Diagnosis of B and T-cell defficiences is by what? | Flow cytometry |
| How would LAD present? | Severe, recurrent and fungal infection with delayed separation of umbilicus. |
| How would LAD present on flow cytometry? | negative CD18 expression |
| What is cheiak Higashi? | autosomal recessive defect in microtubular function and lysosmal emptying of phagocytic cell |
| presentation of Chediak Higashi? | recurrent pyogenic infection with taph,strep, partial albinism and peripheral neuropathy |
| what is CGD | defect in phagocytosis of PMN's secondaryto lack of NADPH oxidase activity. |
| presentation of CGD | recurrent bacterial, viral and fungal infections. |
| Name infection commonly seen in GCD | mmmmmmn |
| how is DX confirmed? | negative nitroblue tetrozolium dye reduction test is indicative of a t dx. |
| All dysfunction of T-cells presents as | skin and mucosal membrane candida infections |
| All dysfunction of B-cells would presents as | deficiency in a specific clas of imunoglobulin. |
| common causes of B-cell deficiency | defective isotype switching |
| wich Ig is frequently deficient? | IgA |
| how does IgA deficiency present? | sinus and lung infections. associated with milk allergies and diarrhea. |
| What is B-cell ataxia telangectasia? | Defecet is in DNA repair enzymes with associated IgA deficiency |
| how else will telangectasia present? | cerebellar problems. ataxia and spider angiomas aka telangectasia. |
| many autoimmune dz pesent with elevated levels of | ab titers |
| what kind of lupus presents with high levels of antihistone? | drug induced SLE |
| Rhumatoid arthritis | Rhumatiod factor- anti-igG |
| vasculitis | antineutrophils, C-ANCA, P-ANCA |
| scleroderma (CREST) | anticentromere |
| scleroderma (diffuse) | anti-scl-70 |
| primary billary cirrhoses | antimitochrondrial (AST/ALT) |
| celiac dz | antigliadin |
| Good Pasture syndrome | antibasement membrane |
| Hashimotor thyroiditis | antimicrosomal |
| Name infection commonly seen in GCD | mmmmmmn |
| how is DX confirmed? | negative nitroblue tetrozolium dye reduction test is indicative of a t dx. |
| All dysfunction of T-cells presents as | skin and mucosal membrane candida infections |
| All dysfunction of B-cells would presents as | deficiency in a specific clas of imunoglobulin. |
| common causes of B-cell deficiency | defective isotype switching |
| wich Ig is frequently deficient? | IgA |
| how does IgA deficiency present? | sinus and lung infections. associated with milk allergies and diarrhea. |
| What is B-cell ataxia telangectasia? | Defecet is in DNA repair enzymes with associated IgA deficiency |
| how else will telangectasia present? | cerebellar problems. ataxia and spider angiomas aka telangectasia. |
| many autoimmune dz pesent with elevated levels of | ab titers |
| SLE | increased ANA (antinuclear) |
| AB that are specific to SLE | anti-ds DNA, antismith |
| what kind of lupus presents with high levels of antihistone? | drug induced SLE |
| Rhumatoid arthritis | Rhumatiod factor- anti-igG |
| vasculitis | antineutrophils, C-ANCA, P-ANCA |
| scleroderma (CREST) | anticentromere |
| scleroderma (diffuse) | anti-scl-70 |
| Good Pasture syndrome | antibasement membrane |
| pemphigus vulgaris | antiepithelial |
| polymyositis dermatomyositis | antijo-1 |
| What cell surface protein show a prediliction for certain diseases. | HLA subtypes |
| psoriasis, ankylosing spondylitis, IBS, Reiters syndrome | show a prediliction for HLA types B27 |
| Graves dz. celiac sprue | HLA types B8 |
| MS, hay fever, SLE, Goodpastures | DR2 |
| DM1 | DR3 |
| DM2, Rhumatoid arthritis | DR4 |
| pernicious anemia, B12 deficiency, Hashimotor thyroiditis. | DR5 |
| Steriod sensitive nephrotic syndrome | DR7 |
| Occurs in minutes ue to preformed ab in transplant recipient against donor antigen | hyperacute rejection |
| occurs weeks after transplant from T-cell response to foreign antigen | acute rejection |
| is acute or hyperacute rejection reversible? | Hyperacute NO! acute Yes! |
| occurs months or years after transplant with ab-mediated vascular damage -fibrinoid necrosis | chronic rejection |
| is chronic rejection reversible? | No! but controlled with steriods/ antirejection |
| What is graft vs host dz? | Grafted Immunocompetent T-cells proliferate in the irradiated immunocompromised host and mount an immune response |
| presentation of Graft vs host dz | hepatosplenomegaly, maculopapular rash and diarrhea. Triad |
| sequale of graft vs ost dz | severe organ dysfunction |
| what is an autograph? | donor is same individual |
| synergenic? | donor is an identical twin |
| allogenic? | donor is genetically different member of same species |
| xenogenic | donor is from another species |
| what type os dz is an exlusively B-lymphocyte mechanism | class switching - humoral division |
| genetic difference of aa in heavy/light chains and have no biologic significance. | allotypic variation |
Created by:
mavis41
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