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Lecture 5

MIMM 214 Lecture 5: MIMM 214 – Lecture 5 – Claire Trottier – Regulation and memory, complement immunity

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

MIMM 214 – Lecture 5 – Claire Trottier – Regulation and memory/complement immunity • Downregulation of t cells and immunological memory • Memory is hallmark of adaptive immunity o Primary response to first exposure to ag ▪ Takes time to develop ▪ Eventually tapers off o Secondary exposure to the same ag ▪ Quicker and stronger response • Why? o Memory lymphocytes o Reactivation yields faster, more significant better response • Note that memory is not in innate immunity • Complement system o Group of soluble proteins o Mostly proteases >30 in blood and other fluids ▪ Protease: an enzyme that performs proteolysis which can break down proteins ▪ Mostly called by “C” followed by # ▪ Some called “factor” followed by a capital letter (factor B) o Complement proteins mostly produced by liver o Set off a chain reaction that helps to amplify inflammation and clear pathogens o Key mech of action ▪ Increasing vascular permeability and chemotaxis ▪ Destroying pathogen cell membranes ▪ Increasing recognition of pathogens and facilitating phagocytosis (opsonisation) • Opsonization and phagocytosis o Opso: coating of surface of pathogen by antibody and/or complement that makes it more easily ingest by phagocytes o Phago: internalization of particular matter by cells by a process of engulfment in which cell membrane surrounds the material, eventually forming an intracellular vesicle (phagosome) containing the ingest material • How does complement get activated? o Components are inactive pro-proteases or zymogens at first o Classical, alternative, lectin pathway o Acting as a cascade ▪ Proteolytic cleavage generating 2 fragments: • 1 small: o Identified by letter a after name (C5a) o With specific function • 1 large: o Identified by letter b after name (c5b) o With proteolytic activity on new substrate • Complement activation essentials o 3 pathways to activate o All converge to generate c3 convertase and cleave c3 to c3a and b to have b bound to microbial surface and releasing a o 3 main outcomes • Lectin pathway o Triggered by prr that circulate in blood ▪ Mannose-binding lectin ▪ Ficolins o Expression of these prrs increases during infection o These prrs can bind to surface of pathogens ▪ Triggers signaling cascade on pathogen surface ▪ C3 convertase is generated and c3 is cleave into c3a and b • Classical pathway o C1q binds pathogen surface ▪ Can bind pathogen directly and bind antibodies that are bound to pathogen
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