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McGill University
Experimental Medicine
EXMD 508

Lecture 1 Main ideasThe Role of Th Cells in IRoT cells from BM go to thymus to mature and be selected and then to lymph nodes to be turned on by BcellsoThe IR must defend from pathgoens survey for abnormal Ag and induce tissue repairoIR respons by infl cells releasing cytokines and chemokines to increase vascular permeability Act as chemotactic agents and change the adhesive properties of the local endothelium this allows the influx of more infl cells into the infection site but is not sufficient to clear the initial resultoInitiation of AIR PRRS on the surface of MphNph Epi releasechemocyto and more infl cells and APC take up Ag and take take it to Lymphnode to present to T cellsoAIR involved B cells releasing AB Cytotoxic T cells that kill nucleated cellsother effectorsoIR Phases can be Immediate Early LateBegin with anonspecific innate response mediated by Phagocyes and NK cellsThen the en the more specific early response that involved more local inflammation and NK mediated Mph activation via IL and then NK cellsIFN Late AIR is more specific with more memory with T cells and AntibodiesTwo arms of theoAIR Humoral and Cell mediated HYmoral involved AB formation by bcells that binds Ag to fascilitate its clearanceThe cell mediated responses involve T cells that recognize Ag presented on self cells Th will responde by making cytokines while Tc will respond by becoming CTLs to mediate the killing of altered self cellsoB cells are kep in check by Th cells T cells allow B cells to progress ALSO Tc cannot divide without Th as well Th regulates both responsesoT LC come from SC in BM andtravel to thymus to undergo CD4CD8 selection Th or Tc oT cells get activated by recognizing peptide Ag in the context of MHC Tc restricted by MHC1 Th by MHCII ag get taken up by phagocytic cells broken down and shunted into pockets called MHCDevelopment of Th Cell PathwaysoPeptide recognition in the context of MHC induce Th cell activation differentiation depending on type of effector immune Response Also their own IL2 production to allow theirexpansion The Th cells will then communicated with b cells and induce their division into memory of plasma while the Tc will kill altered state cellsThcell differentiation depends on thecytokines it is exposed to All these signals for Th differentiation come from APC SIGNAL 3Th1 IFNgIL12 Th2 IL4 Th17 IL6Treg IL2 But these Reg Ts are uindueced initially by TGFB Most Dammaged cells release TGFB and IL6more Th17 that attract Nph T cell can be Th1 Th2 Th17 Treg IFNg and IL12 work together to initiate an Th1 response via STAT1IL4 induces a TH2 response viaand releases ILs 5 13 4 to STAT 6compete with IFNg action and thus inhibit Th1 productiionTGFB induces Treg devo with IL6 becomes Th17THESE TGFB for TREG IL12IFNg for TH1 IL4 for TH2 that releases 5 13 4 to prevent Th1All these signals for Th differentiation come from APC SIGNAL 3CD4 vs CD8 CD4 t cells or Th cells have various functionsIFNgIL12Th1Mphrecruit and release inf lmediatorsinc adhesion moleculesinc monocyte production by BMMycoBacteria In vesiclesMHCIIAg will Activate CD4 Th1 CellsCKMPH recruiting IFNg Mph infl mediators TNFa BV adhesiveness IL3 GMCSF Monocytes diff from BMIL4Th2 B cellto cause AB class Switching IgM to IgA to attain memory and cross muscosal barriersalong with maintained IgG for EC infections Some IGE as well but proproblematicr allergies but signals infection to CNSparasites Allergic responseAB Opsonize for Mph targeting Block harmful Ag and activate ComplementTh2 Activates B cells by making IL4 and CD40 reorient cytoskeletonTGFB IL6Th17 RECRUIT NPH downregulate Th response more antimicrobial peptides EC BACTERIA And FungiBUT TH17 CONTRIBUTES TO CHRONIC INFLVIRAL REPfavorable
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