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Adaptive Immune Response, T-cell Receptor -does not bind antigen directly like ABs,BCR -binds fragments presented on MHCs ->recognize Ags displayed on body's own cells -similar to Fab of AB-both disulfide-linked heterodimers -contains hinge, hydrophobic transmemb, cytosolic tail -contain V_alpha, C_alpha, V_beta, C_beta (not HvsL) (some w/ gamma:delta chains) -ONLY one antigen-binding site (not 2 like BCR) -NEVER secreted -SHORTER AND WIDER than Fab -carbs on TCR, not on Fab -less flexible hinge b/c more interaction b/w chains Diversity alpha-chain--80 V_alpha, 61 J_alpha beta-chain-ᡬ V_beta, D_b1,2, 6Jb1, 7Jb2,Cb1,2 3 CDRs on each chain-interact w/ peptide:MHC CDR1,2 less variable->bind less variable MHC CDR3 more variable-bind peptide (from D,J genes), Lymphocyte Receptor Generation ~10^11 diff AB specificities -due to germline and somatic diversification theories ->many genes, then alteration somatic recombination-V and C region on same DNA fragment in B cell -separate in germline junctional diversity-splicing variation/inaccuracies H and L chain random assortment combinational diversity-V,D,J joining-use RAGs somatic cell mutation during maturation of immune resp. -responding B cells mutate by trial & error, +/- selection -uses AID N region diversity-by terminal deoxynucleotidyl transferase V region V Heavy Chain-3 segments V_H,D_H,J_H 40 V_H, 25 D_H, 6J_H, Lymphocyte Receptor Generation ~10^11 diff AB specificities -due to germline and somatic diversification theories ->many genes, then alteration somatic recombination-V and C region on same DNA fragment in B cell -separate in germline junctional diversity-splicing variation/inaccuracies H and L chain random assortment combinational diversity-V,D,J joining-use RAGs somatic cell mutation during maturation of immune resp. -responding B cells mutate by trial & error, +/- selection -uses AID N region diversity-by terminal deoxynucleotidyl transferase V region V light chain-2 gene segments -V(most of region) and J (join) segments 40 kappa, 30 lambda clustered at V loci +5J, 4J, Immunoglobulins-B cell AG-recognizers -contains 2 each of 2 diff chains Heavy (H) Chain-defines Ig class, 50kDa -constant region-carboxy terminus mu-IgM-form pentamers-MACROGLOB gamma-IgG MOST ABUNDANT alpha-IgA-can form dimers epsilon-IgE delta-IgD-unknown fcn -have N-linked carb. groups Light (L) Chain (must have 2 of k or l) kappa:lambda = 2:1 ~25kDa each thus IgG can be gamma_2kappa_2 CH2 domains not paired, unlike all others Hinge-molecular ball-and-socket joint Ig Isotypes -IgM, IgE lack hinge region -still flexible -IgM, IgE w/ extra C domain -disulfide bonds differ in all -even diff. C-region genes 4 gamma, 2 alphas, 1-others, Immunoglobulins-B cell AG-recognizers -contains 2 each of 2 diff chains Heavy (H) Chain-defines Ig class, 50kDa -constant region-carboxy terminus mu-IgM-form pentamers-MACROGLOB gamma-IgG MOST ABUNDANT alpha-IgA-can form dimers epsilon-IgE delta-IgD-unknown fcn -have N-linked carb. groups Light (L) Chain (must have 2 of k or l) kappa:lambda = 2:1 ~25kDa each thus IgG can be gamma_2kappa_2 CH2 domains not paired, unlike all others Hinge-molecular ball-and-socket joint Variable Region Similar, but larger than C region -both made from 2 beta-sheets V region -contains 4 framework regions (FR1-4) -contains 3 complementarity-determining regions (CDR1-3) on each VL and VH -hypervariable loops -VH+VL=>antigen binding site -6 CDRs-combinatorial diversity -makes unique pockets for specific AAs, size, shape of antigen -conformational epitope holds antigen via reversible, non-covalent forces-direct Ig:Intact AG interaction, Ag fragment presented on MHC molecules -peptide fragments that were deep w/in Ag -whereas BCRs bind surface peptides TCRs interact w/ MHC and peptide in cleft MHC I and II expression regulated by cytokines -esp. IFNs -IFN-gamma->increase expression -IFN->enhance Ag presentation on Class I MHC Structure Class I and II sim. overall structure -furthest pair of 4 subunits has cleft -both stabliized by peptide-binding -peptide loss->denaturation -peptides seldom leave MHC -stably bind many diff peptides -if uninfected->MHC to surface w/ "self" -highly polymorphic among species -small selection per person, Lymphocyte Receptor Generation ~10^11 diff AB specificities -due to germline and somatic diversification theories ->many genes, then alteration somatic recombination-V and C region on same DNA fragment in B cell -separate in germline junctional diversity-splicing variation/inaccuracies H and L chain random assortment combinational diversity-V,D,J joining-use RAGs somatic cell mutation during maturation of immune resp. -responding B cells mutate by trial & error, +/- selection -uses AID N region diversity-by terminal deoxynucleotidyl transferase Secreted vs. membrane-bound Igs Alternative mRNA processing SC contiguous w/ last C domain exon for all but IgD for secreted, cleave membrane-coding (MC) exon -post poly-A tail -keep secretion-coding (SC) exon for membrane bound-excise SC, keep MC -poly-A tail after MC, Immunoglobulins-B cell AG-recognizers -contains 2 each of 2 diff chains Heavy (H) Chain-defines Ig class, 50kDa -constant region-carboxy terminus mu-IgM-form pentamers-MACROGLOB gamma-IgG MOST ABUNDANT alpha-IgA-can form dimers epsilon-IgE delta-IgD-unknown fcn -have N-linked carb. groups Light (L) Chain (must have 2 of k or l) kappa:lambda = 2:1 ~25kDa each thus IgG can be gamma_2kappa_2 CH2 domains not paired, unlike all others Hinge-molecular ball-and-socket joint Cleaving Pepsin cuts on carboxy side of hinge -makes F(ab')_2, Ag fragment presented on MHC molecules -peptide fragments that were deep w/in Ag -whereas BCRs bind surface peptides TCRs interact w/ MHC and peptide in cleft MHC I and II expression regulated by cytokines -esp. IFNs -IFN-gamma->increase expression -IFN->enhance Ag presentation on Class I MHC Structure Polymorphism on MHC Class I and II -everyone is heterozygous at each locus -co-dominant expression (express both MHCs) -eg, has 2 diff alleles for each Class I-A, B, C ->difficult to match organ donor Polymorphism+Polygeny=eg, 6 diff MHC-Is -variation occurs at binding cleft -on alpha_1 and alpha_2 in MHC-1-line cleft -only on beta_1 chain in MHC II, Ag fragment presented on MHC molecules -peptide fragments that were deep w/in Ag -whereas BCRs bind surface peptides TCRs interact w/ MHC and peptide in cleft MHC I and II expression regulated by cytokines -esp. IFNs -IFN-gamma->increase expression -IFN->enhance Ag presentation on Class I MHC Structure Class II-two chains -both alpha and beta span membrane 9 Polygeny-3 loci HLA-DP,DQ,DR alpha/beta -both MHC-encoded -alpha1, beta1 form cleft -more open than class I ->peptide ends exposed -binds longer peptides (ᡅAA) -binds along length, can emerge from groove -peptidases clip to 13-17 AAs -also contains anchor residues, not at ends