MIMM 214 Final: Final Exam Review

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McGill University
Microbiology and Immun (Sci)
MIMM 214
Claire Trottier

Tuesday, April 11, 2017 1:46 PM Complement: 3 activationspathways Classical: C1q Connects adaptive to immune (bc C1q can bind Ab, IgMIgG) Lectin Triggered by PRRs that circulate in bl: annosebinding lectin, Ficolins C3 convertase cleaves C3 into C3a C3b Alernative (spontaneous hydrolysis) Need C3b from lectinclassical pathway Spontaneously occuring from convertases in plasma 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 C3b helps phagocytosis (opsonization) Need to know: how each pathway is activated, how they follow through, what are the effector functions INFLAMMATION C3a C5arecruit phagocytes, promote inflammation Too much C3a C5a would cause naphylactic shoc, and death INCREASED PHAGOCYTOSIS Via opsonization Phagocytes have receptors for C3b PATHOGEN LYSIS Membraneattack 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 FkB IRF3 MAPK, which go into the nucleus) Recall slide with all the different signalling pathways, last molecules are NFkB etc. MyD88 TRIF = adaptor proteins (bind to PRRs) Innate immunity antigen presentation: Endogenous pathway (MHC I)p : olyubiquitination => proteasome degredation
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