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Immunology!
UCI SOM Gutman
| Question | Answer |
|---|---|
| APC | antigen processing cells (all are phagocytic) |
| Lymphoid tissues | lymph nodes, spleen, peyers patches et al, thymus, bone marrow, travel via the blood and lymph |
| Iatrogenic | illness brought on by healer |
| Innate immunity | no adaptive specificity, no memory, mucous membrane, phagocytes, complement, anti-bacterial peptides |
| Adaptive immunity | specificity, memory, B and T cells |
| Humoral immunity protects from what | protection from extracellular parasites (antibody mediated); test is if you can transfer immunity by injecting serum into a host |
| Cell-mediated immunity protects from what | protection from intracellular parasites |
| Active immunity | host creates own antibodies |
| Passive immunity | antibodies are injected into host (not created by host) |
| Challenge | the act of giving the host an antigen to see if it’s immune |
| Afferent limb | where antigen uptake and processing takes place |
| Central limb | where proliferation and differentiation takes place (formed in formal lymphoid tissues) |
| Efferent limb | where target killing, tolerence, etc. occur |
| Epitope | (=antigenic determinant) minimum target structure to which Ab binds |
| Immunogen | elicits immune response |
| Hapten | small molecule that, when combined to a larger molecule, will elicit an immune response |
| Adjuvant | any material that increases the immunogenicity of some antigen (the water/oil antigen thingy) |
| Physical manifestations of an antibody | precipitation for soluble Ag, agglutination for particulate Ag, and binding |
| Biological effects of antibodies | protection, immobilization, cytolysis, opsonization |
| Equivalence | point of most precipitate on the precipitin curve |
| Prozone effect | antibody excess on precipitin curve resulting in less precipitation |
| Ouchterlony | place antigen and antibody away from eachother in agarose gel and see where they precipitate (reversible) |
| Radial immunodiffusion | place antigen in antibody and measure the diameter of the circle of precipitate to see how much lysis occured |
| SRBC | sheep red blood cells |
| Reverse agglutination | latex coated with antibody; antigen is added (way to check which antigen it is) and agglutination is checked |
| Serological | typed by antibodies |
| Passive hemagglutination | place antigen and antibody in many test tubes and see which ones clump on bottom (no agglutination b/c the antigens can roll over eachother to get to the bottom of the test tube) or which ones agglutinate and therefore have a broad smear across the bottom |
| ELISA | Enzym-Linked ImmunoSorbent Assay; Ag is bound to plate, antibody is labeled with a visible dye |
| Electrophoresis of normal serum (proteins from + to -) | albumin (most negative; closest to +), alpha 1, alpha2, beta, gamma (short, broad peak near zero) |
| Bruton’s disease | x-linked; impaired maturation and development of antibodies (B-cell defect) |
| RIA | RadioImmunoAssay (used radioactive isotopes); same as ELISA except ELISA is safer and currently used |
| Equilibrium dialysis | used to analyze the binding of Ab to Ag and to determine valency and strength of binding |
| Papain | cleaves IgG into 2Fab and Fc |
| Pepsin | cleaves IgG into F(ab)2 and Fc (degraded) |
| What does ab stand for in Fab | antigen binding |
| What does c stand for in Fc | crystallizing |
| What determines the class and subclass of an antibody | heavy chain |
| Light chain types | kappa and lambda |
| # of IgG subclasses, # binding sites, H-chain classes, and biological properties | 4; 2; gamma 1, 2, 3, 4; c-fixing, placental x-fer |
| # of IgM subclasses, # binding sites, H-chain classes, and biological properties | 0; 10; mu; c-fixing, B-cell surface Ig |
| # of IgA subclasses, # binding sites, H-chain classes, and biological properties | 2; 2,4,6; alpha 1, 2; secretory Ig |
| # of IgD subclasses, # binding sites, H-chain classes, and biological properties | 0; 2; delta; b-cell surface Ig |
| # of IgE subclasses, # binding sites, H-chain classes, and biological properties | 0; 2; epsilon; reaginic Ig |
| Order of concentration in Igs in serum | G>M>A>D>E; found in mg/ml |
| Size of IgG | 150 KDa |
| Monoclonal proteins | myeloma proteins and Bence-Jones Proteins (L-chains) |
| Monoclonal gammopathies | occurs when a certain immunoglobulin becomes homogenous |
| CDR | complementarity determining region (hypervariable region of variable region of Igs) |
| Affinity maturation | progression in the affinity of an Ig for its antigen over time |
| complement | group of serum proteins activated by ag=ab complexes resulting in lysis or other stuff |
| which complement proteins have cytolysis ability | C5b6789 |
| which complement proteins have anaphylotoxin activity | C3a, C5a |
| which complement proteins have chemotaxis activity | C5a, C5b67 |
| Which complement proteins have opsonization activity | C3b |
| Which complement proteins have tissue damage ability | C5b6789, PMN's |
| MAC | membrane attack complex; all 3 complement pathways can produce MAC |
| how is the classical pathway activated | heat |
| complement pathway steps 1-5 | 1)S+A->SA 2)C1q, C1r, C1s->C1qrs 3)SA+C1qrs->SAC1qrs 3)C1qrs+C4->C1qrs/4b+C4a 4)C1qrs/4b+C2->C1qrs/4b2b+C2a 5)C4b2b+C3->C4b2b3b+C3a |
| complement pathway steps 6-9 | 6)C4b2b3b+C5->C4b2b3b5b+C5a 7)C4b2b3b5b+C6+C7->C4b2b3b5b67 8)C5b67+C8->C5b678 9)C5b678+C9->C5b6789 |
| convertase | can cleave a complement protein |
| alternate pathway | 1)B+C3b->BbC3b+Ba 2)BbC3b+P->PBbC3b 3)PBbC3b+C3->PBb(C3b)2+C3a which can fix C5, C6 etc. |
| what triggers the alternate pathway | microorganisms, parasites, aggregated immunoglobulin |
| MBLECTIN pathway | 1)MBLECTIN+mannan->MBLECTIN/mannan/MASP-1/MASP-2 which is a C4 convertase |
| advantages/disadvantages of alternate and MBLECTIN pathways | don't need Ab to work; not very good specificity and no memory |
| final effects of complement | lysis, opsoniziation and inflammation |
| Immune complex disease | Ag-Ab complexes binding the bloodstream to blood vessels and kidney glomeruli |
| one-shot serum sickness | immune complex disease that goes away quickly because the antigen is a one-shot activity; if the antigen is normal tissue, autoimmunity ensues |
| how many kappa genes | 1 |
| how many lambda genes | 4 |
| how many heavy chain genes | 9 |
| allelic variants of immunoglobulin genes | Km, G1m, G2m, G3m, G4m, Em, A2m |
| how many isotypes of ig's are there; how many does each person have | 14 different isotypes present in all humans |
| allotype definition and how are they inherited | allelic variants within constant regions; inherited in mendelian co-dominant fashion |
| idiotype | unique combination of Vh and Vl |
| clonal selection/expansion | the proliferation of antibody cell specific to a certain antigen |
| affinity maturation | as a response progresses, the antibodies with higher affinity will be selected |
| combinatorial joining | joining a random V-region with one of the 5 J-segments in Kappa or several D-segments in heavy chain |
| combinatorial association | random association of H- and L-chains |
| germ-line theory | for every kappa-chain V-region, there exists one unique germ-line gene |
| somatic theory | only one germ-line gene exists and somatic mutation accounts for all kappa-chain v-regions |
| on what chromosome are the kappa genes | 2 |
| on what chromosome are the lambda genes | 22 |
| on what chromosome are the heavy chain genes | 14 |
| j-segments | piece on a kappa chain between the V and C regions |
| what two immunoglobulins can be produced simultaneously and continuously by B-cells | IgM and IgD |
| what determines whether an Ig is execreted versus in a membrane-bound form | alternate mRNA splicing |
| TCR | T-cell receptor |
| 3 differences in structure/expression of TCR's compared with Ig | 1)TCR has a single combining site 2)somatic mutation does not occur in TCRs 3)TCR's only exist as membrane-bound molecules |
| RAG-1 and RAG-2 | two recombinase enzymes necessary for TCR and IgR V(D)J recombination; knock-out of RAG proteins leads to inability to produce mature T and B cells |
| kappa gene structure | V(n), J, C |
| lambda gene structure | V(n), J, C1, J, C2, J, C3, J, C7 |
| heavy chain gene structure | V(n), D, J, Cmu, Cdelta, C gamma till ends with Calpha2 |
| CMI | cell-mediated immunity |
| what produces most immunoglobulins | plasma cells |
| ratio of H and L-chains in normal plasma levels as opposed to myeloma cells | similar ratio in normal cells; way more L-chains in myeloma cells (these become bence-jones proteins) |
| where does carbohydrate add onto (not the Asn, but what part of Ig) the Ig in normal cells | only H-chain (myeloma cells put them on Vh and Vl) |
| when and to whom is the J-chain added | just prior to being secreted; on IgM and IgA |
| IgA secretion 4 steps | 1)(IgA)2 or 3 is secreted into extracellular space 2)epithelial cells have S-piece precursor that binds IgA 3)IgA with Sp is transported to the other side of epithelial cell, Sp is cleaved into 2 pieces 4)IgA with one part of Sp is secreted into lumen |
| how many idiotypes does one AFC produce | 1 |
| allelic exclusion | for every immunoglobulin gene in a B-cell or plasma cell, only one allele is expressed |
| heavy chain class switching; can you go backwards? | M to D to G to A to G to E to A; you cannot go back |
| how are membrane IgM's and free IgM's different | C-terminal sequence; no J-chain on membrane IgM's and they are therefore monomeric |
| what does a virgin B-cell only produce | membrane-bound IgM |
| difference among virgin B-cells, memory B-cells, and plasma cells | virgin B-cells produce only membrane-bound Ig's; virgins turn into memory B-cells after first antigen and produce membrane bound and secretory Ig's; these become plasma cells after second antigen stimulation and only secrete Ig's |
| why start with IgM | its avidity compensates for lack of affinity but it is very expensive to make; as person develops, she can make IgG's with higher affinity and with less cost |
| erythroblastosis fetalis | results from infants blood reaching the mother's bloodstream during birth, creating antibodies and those antibodies attacking the next child |
| isoagglutinins | natural antibodies against whichever of the A and B antigens is not present in that persons RBCs |
| crossmatching | mixing donor RBCs with acceptor RBCs to make sure it will work |
| stem carbohydrate structure, B structure, A structure | RBC—O-GLU(-Nac)-GAL-FUC; B has a GAL on the stem's GAL; A has a NAc on B's extra GAL |
| what class of Ig's are made against foreign blood groups | IgM |
| % of population that is Rh- | 15% |
| % of population that is A, B, AB, O | 40%, 10%, 5%, 45% |
| what kind of natural antibodies do we have against Rh | NONE |
| HDN | hemolytic disease of the newborn (same as erythroblastosis fetalis) |
| exchange transfusion | total replacement of infant's blood to remove the anti-Rh antibodies and provide undamaged RBCs |
| RhoGam | anti-Rh antibody injected into the mother so that she doesn't develop them so as to stop erythroblastosis fetalis |
| MHC | major histocompatibility complex; HLA in human, H-2 in mouse |
| HLA | human leukocyte antigen system is the name of the MHC in humans |
| first set rejection | primary immune response to a graft (the first rejection) |
| isograft/syngeneic graft | graft from a genetically identical individuals |
| allograft | transplant from one individual to another with a different genotype |
| second set rejection | second rejection to the same graft but is much quicker |
| is graft rejection a cell mediated or humoral mediated immunity | cell mediated |
| what can transfer only humoral or only cellular immunity | serum can only transfer humoral, but nothing can transfer just cellular |
| immunological enhancement | when circulating antibodies protect a graft from rejection |
| what are the antigens triggering graft rejection | cell surface glycoproteins=histocompatibility complex |
| HLA class I and class II genes | I-A,B,C (these are SD); II-D (DP, DQ, DR) (these are LD) |
| H-2 class I and class II genes | I-D,L,K II- I-A, I-E |
| Ir genes | immune response genes which encode class II antigens (specifically in mice) |
| SD | serologically determined (type I in HLA) |
| LD | lymphocyte determined (mixed lymphocyte reaction) (type II in HLA) |
| which cells express class I antigens | all nucleated cells |
| which HLA class is the major target for graft rejection | class I |
| do all cells express class II | NO |
| class III genes | C2, C4, and B (S in mouse) code for complement components |
| what do class II molecules do | required for the process of antigen presentation to helper T-cells |
| graft-versus-host reaction | the graft attacks the host |
| 3 conditions of graft vs. host rxn to occur | 1)graft must contain immunocompetent cells 2)graft must be capable of recognizing foreign antigens on host tissue 3)recipient must be incapable of rejecting the grafted tissue |
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