Immunology/Inflammation - MAGL
The innate immune system is triggered when microbial pathogens are targeted by pattern recognition receptors such as Toll-like receptors (TLRs) that recognize the pathogen-associated molecular patterns. The activated TLRs initiate a cascade of interaction between various intracellular signaling adaptors including MyD88, IRAKs, and TRAF6, resulting the activation of the MAP kinase, NF-κB, and IRF signaling pathways, which mediate inflammation through the production of inflammatory cytokines, chemokines, type I IFN, and antimicrobial peptides.
The adaptive immune system consists of B and T lymphocytes which mediate humoral immunity (e.g. antibody response) and cell-mediated immunity, respectively. B cell receptor and T cell receptor signaling is responsible for activation of Src family tyrosine kinases, such as Blk, Fyn, and Lyn in B cells and Fyn and Lck in T cells, resulting phosphorylation of the receptor-associated ITAM motifs. Phosphorylated ITAMs serve as the docking sites for Syk family tyrosine kinases, e.g. Syk in B cells and Zap-70 in T cells. Activated Syk kinases then propagate the signals via phosphorylation of downstream proteins. Furthermore, lymphocyte receptor signaling facilitates B and T cell development, differentiation, proliferation and survival.