T cell maturation/act/diff Positive/negative selection in thymus This is after gene re arrangement P56K, a protein kinase initiates S.D.

Anergy will ensue if not enough IL-2 is made B Cell Mat/act/diff Immature B cell leaves BM with IgM Will mature to have both mIgM and IgD with one specificity Pro B cells proliferate in BM, express membrane CD45R Need stromal BM cells to become Pre-B cells They secrete IL-7 Heavy chain re arrangement in Pro B stage Becomes Pre B when it has heavy chain Nave B cells seek out humoral Ag with their mIgG and endocytose it, and present it on MHC2 for Th2 help TCR of Th2 binds to MHC 2 on B cell but needs a co receptor CD40 and CD40 Ligand on TH2 Nave B cells are in the G0 stage Complement c3d, binds to Ag on mIGM and acts as a co receptor Binding of an Ag can lead to increase of affinity of total b cell population. B cells help their Th helpers help! B cells are great APCs when there is little Ag Bcells can proliferate without Th2 (TI pathway) but need TH2 to differentiate from IgM IL-2.4.5 are needed for B cell Differentiation

TCR CD3 is on TCR and helps start signal transduction after TCR binding on MHC Tails of CD3 have motif called ITAM for S.D. CD4/8 are co-receptors which increase affinity TCR affinity is weak compared to BCR Uses CAM to initially bind to APC target cell MHC CD28 on Tcell and B7 on APC bind and initiate S.D. Cytokines TH1: IL2,3, IFN-y, TNF-b. Mac, Tc activation. DTH act. TH2: IL3,4,5,10. Ab , Eosinophil, mast cell production Cross Regulation: Th1 inhibits Th2 and vice versa Th1 production needs IFN-y and T-Bet transcription factors Th2 production needs IL-4 and GATA-3 transc. Fact. IL-10 released from Th2 inhibits Macs from activating Th1 consequently inhibiting CTL Cytokines involved in: GF, DF, signaling Cytokine needs a receptor which needs a tail to send signal via transduction for gene expression Cytokine binding increases cytokine receptor/affinity CMI Nave T cells require CD28-B7 co stimuli-effectors do not require it. Effectors have high CAMs Effector molecules made by effector cells CTL: cytotoxins (perforin and granzymes) IFN-y, TNF-B and membrane bound FAS TH1: IL2,3, TNF-B, IFN-y, GM-CSF TH2: IL-3,4,5,6,10,13 and membrane CD40 ligand Along with MHC recognition, need co stim by CD28/B7 and IL2/IL2R on CTL membrane

Hypersensitivity Type 1: atopy Plasma cells secrete Ige in response to allergen specific Th2 cells Ige binds to Fc receptors on mast cells Later exposure to same Ag cross links Ige on surface of mast cells inducing degranulation DTH APC presents intracellular pathogen to Th cell Becomes Th1 cell Th1 cell secretes Il2, INF-y which recruites activated Macs, not neutrophils Macs now have increased killing and APC Macs secrete IL-12, recruiting more Thelp, increaseing whole reaction. Mycobacterium tuberculi blocks phagolysosomal fusion rendering Mac useless. When Activated Macs arrive, they kick some ass because of NO, free radicals, etc This is a CMI response, not humoral