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Humoral Immunity, Humoral Immunity B cell Activation -requires 2 signals Signal 1->Ag:B cell binding -then internalized->MHC-II Co-receptor-CD19:CD21:CD81 -CD21:C3dg->induce AB at 10,000x smaller doses 2. Thymus-Independent (TI) Ags -eg bac. polysacchs 2nd signal on microbe OR -massive B cross-linking from binding epitopes on same bac., IgG- -transported across placenta via FcRn Activate Complement Pentameric IgM-bind bac surface -C1q binds to whole IgM molec IgG-bind to antigens on surface -C1q binds at leaast 2 IgG molecs ->activate C1r->activate C1s C3b all over bac-bind CR1 on RBCs -transport to spleen for removal, When GC forms->'secondary follicle' -rapid B cell prolif-kept alive via BCR, CD40 B cell reactions: 1. Somatic hypermutation-alter Ig V-regions -subtle differences->most not improved->apop ->uptake by dark macs (tingible body macs) 2. Affinity maturation-survival of Bs w/ high Ag aff 3. Isotype switching ->differentiation to 1. Plasma cell-secrete ABs -leave GC to med. cords or bone marrow 2. Memory B cells-circulate through secondary lymphoid tissue, splenic marg. zone Antibodies IgE-at body surfaces -crosslinking degranulates mast cells ->increase lymph flow to DLN ->trigger musc contraction->expel pathogen -also for parasitic infections, B cells w/ Ag go to B/T border in Spleen/LN -Trapped T and B interact, activate -B migrate out to proliferate in -marginal sinus (spleen)->primary foci-immed response -medullary cords (LN)->primary foci -primary follicle->form germinal center ->B cells diff'ate into Plasmablasts -secrete ABs, but otherwise like resting B ->diff'ate into Plasma Cell-high Ig secretion -no surface MHC-II,Ig,growth,isotype switching -terminal cell, no longer APC Primary Follicle Contains resting B cells and Follic DCs -and 10% Ag-specific T cells -B cells clustered around FDCs FDCs release CXCL13 ->recruit naive and activated B cells, 2. Thymus-Independent (TI) Ags -eg bac. polysacchs 2nd signal on microbe OR -massive B cross-linking from binding epitopes on same bac. TI-2 Ags -infants don't respond well to TI-2 Ags -TI-2 only activate MATURE B cells -mostly B-1 cells ->multiple cross-linking of BCR ->IgM production by B cells -TI-2 Ab concen. can't be too high->anergy T cells can release cytokines ->inc. AB production by B cell -and isotype switching to IgG but for LPS bac, opsonization needed for phagos to eat pathogen->APC to T cell->augment TI-2, 1. Thymus-dependent Ag(TD Ags) -TH bind via CD4:MHC-II ->CD40L(T cell):CD40(B) -2nd signal -'linked recognition'-B and T respond to same Ag -could be diff epitopes T and B bind-LFA-1(T):ICAM-1(B)-seals ->polarize cytoskeleton ->TH2 releases IL-4 after MHC recognition ->clonal expansion of Bs (w/ CD40) CD40 (TNFR family)-no Death Domain ->enter into cell cycle, make B7 co-stims Isotype Switching B cell switches C region of AB -from M,D to others -CD40:CD40L binding necessary (k/o mice w/ hyper-IgM syn-> recurrent infections) IL-4->switch to IgG1, IgE IL-5->augment IgA IFN-g (from TH1 cell)->IgG3,IgG2a TGF-b->induce IgG2b, IgA, 1. Thymus-dependent Ag(TD Ags) -TH bind via CD4:MHC-II ->CD40L(T cell):CD40(B) -2nd signal -'linked recognition'-B and T respond to same Ag -could be diff epitopes T and B bind-LFA-1(T):ICAM-1(B)-seals ->polarize cytoskeleton ->TH2 releases IL-4 after MHC recognition ->clonal expansion of Bs (w/ CD40) CD40 (TNFR family)-no Death Domain ->enter into cell cycle, make B7 co-stims H. influenzae Make vaccine w/ capsular polysacchs -attach to tetanus toxoid (infants already vacc. against tetanus) -B cell recognizes poly sacch. -2nd signal from Tcell (recognize tet) ->B cel makes AB against polysacch., Bind toxin to prevent cell binding -need quick-diffusing Igs ->IgG, IgA-high affinity Also bind viruses to prevent endocytosis And block bac adherence to lympho anti-pilin (gonorrhea adhesion) IgA IgG-for toxins in tissues IgA-for toxins in mucosa NK cells can bind IgG via Fc -cross-link Fc->NK active->kill cell Removal Bind to Fc receptors -on accessory effector cells -bind to C region -diff Fc receptors on diff cells -cross-link receptors ->activate macs, When GC forms->'secondary follicle' -rapid B cell prolif-kept alive via BCR, CD40 B cell reactions: 1. Somatic hypermutation-alter Ig V-regions -subtle differences->most not improved->apop ->uptake by dark macs (tingible body macs) 2. Affinity maturation-survival of Bs w/ high Ag aff 3. Isotype switching ->differentiation to 1. Plasma cell-secrete ABs -leave GC to med. cords or bone marrow 2. Memory B cells-circulate through secondary lymphoid tissue, splenic marg. zone Antibodies IgM-produced first -no isotype switching necessary -low affinity, but forms pentamers ->higher avidity -mainly in blood b/c bigger ->activate complement, Contains resting B cells and Follic DCs -and 10% Ag-specific T cells -B cells clustered around FDCs FDCs release CXCL13 ->recruit naive and activated B cells Germinal Center- -for more effective later response Histology-B cell proliferation in both Light,Dark Dark zone-contains centroblasts -rapidly prolif B cells w/ little surface IgD Centrocytes-dec. division rate, more surface Ig Light zone-w/ FDCs and more developed B cells Mantle zone of resting B cells at edge