Immunology 18 - Immunology 18-Immune Dynamics and Memory 1...

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Immunology 18-Immune Dynamics and Memory 1. Establishment of infection; threshold level of Ag to activate adaptive immune response 2. Induction of adaptive response (pathogen level still increasing) 3. Adaptive immune response 4. Immunological memory Innate immunity is absolutely essential Th17 vs Treg differentiation: Treg— inhibitory ; produces TGF B and IL-10; in the absence of infection, DCs make predominantly TGF-B and LOW level of IL-6→CD4 T ells are activated to express FOXP3 and show a regulatory phenotype; inhibit TH1/TH2 differentiation Th17— extracellular bacteria : Induced by IL-23 (provides proliferative signals; source= activated DCs); infection induces Dcs to express HIGH levels of IL-6; naive T cells respond by expressing RORγT and becoming Th17 cells Produce IL-17; acts on stomal cells to: Increase IL-6 (positive feedback); increase CXCL8, CXCL12 (neutrophil recruitment); increase GM-CSF, G-CSF (neutrophil and macrophage activation) TfH cells= have the transcription factor Bcl-6 Th1 differentiation Intracellular pathogens Induced by IFN-y (source= NK, NKT, CD8 T cells); expanded by IL-12 (support/expansion; source= DCs, macrophages, TLR activation); viruses and some bacteria induce IL-12 secretion by DCs that can activate NK cells to produce IFN-y→ naive CD4 T cells, activated in the presence of IL-12 and IFN-y, respond by expressing T-bet and are committed to differentiate into TH1 cells Effector mechanisms: activation of CD8 T cells (licensing step); activation of phagocyte killing mechanisms (macrophage); class switch to IgG2a, IgG3 Produce: IL-2, IFN-y and TNF-B **IL-12(TH1) and IL-23(TH17) share a p40 subunit and their receptors share the IL-12RB1 subunit; differ in what small subunit they associate with; IL-12: P40 associates with p35 and activation of STAT 4; IL-23: P40 associates with p19 and activation of STAT 1, 3 and 5 Th2 differentiation Extracellular parasites? Induced by IL-4 (source= iNKT, mast cells, basophils, Th2 T cells); other pathogens (worms) may cause the synthesis and secretion of IL-4 by NKT cells→ naive CD4 T cell respond by expressing GATA3 and commit to differentiate into TH2 cells Effector mechanisms: drive class switch to IgE, IgG1 Produce: TGF-B and IL-10 ** innate recognition produces cytokines needed to induce adaptive immune response Different sets of cells cross regulate eachother Signals aren’t binary (on/off); stoichometric differentiation (not all or none); “tend” to become on cell or the other Spectrum: usually cells fall between these subtypes; cytokines are a suggestion rather than a command Effector T cells Reprogrammed to home to different sites: No longer home to secondary lymphoid tissue: decrease L-selectin (CD62L); decrease CCR7 (T cell zone) Home to peripheral sites (sites of inflammation): modified PSGL-1 (ligand for endothelial P and E selectins); increased α4 integrins (α4:β1
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This note was uploaded on 02/08/2012 for the course PATHOLOGY 3245 taught by Professor X during the Spring '11 term at UWO.

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Immunology 18 - Immunology 18-Immune Dynamics and Memory 1...

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