MIMM 214 Final: Final Exam Review
12 May 2017
School
Department
Course
Professor
Document Summary
Connects adaptive to immune (b/c c1q can bind ab, igm/igg) Triggered by prrs that circulate in blood: mannose-binding lectin, C3 convertase cleaves c3 into c3a & c3b. Or, c3 undergoes spontaneous hydrolysis (c3 --> c3b + c3a), then the c3b will join the c3 convertase, which cleaves c5 --> c5b + c5a. No matter which pathway, they all converge through c3 convertase => c3a + c3b. Need to know: how each pathway is activated, how they follow through, what are the effector functions. Too much c3a & c5a would cause anaphylactic shock, and death. Membrane-attack complex (mac) forms, punching a hole in the pathogen membrane, causing cell lysis. Lots of prrs recognie a strutucrally diverse set of pamps, but converge onto a limited number of signaling pathways (nf-kb & irf3 & mapk, which go into the nucleus) Recall slide with all the different signalling pathways, last molecules are. Myd88 & trif = adaptor proteins (bind to prrs)
