MIMM 214 Lecture 5: Innate Immunity I: Regulation and Memory
7 Feb 2017
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Document Summary
Memory is hallmark of adaptive immunity: primary response to first exposure to ag, takes time to develop, eventually tapers off. Immediately available and does not get better with exposure: mostly mediated by leukocytes other than lymphocytes (e. g. macrophages, dendritic cells, no fine specificity, link made by dcs (or other apc) which activates adaptive cells in lymphoid tissues. Spleen, in gut, lymph nodes: adaptive (aka acquired) immunity, ag-specific, mediated by lymphocytes (e. g. t and b cells) These cells express specific receptors: clonal selection, humoral and cell mediated. Innate immunity module: complement: content, complement, anatomic barriers & initial defense, pattern recognition. Set off a chain reaction that helps to amplify inflammation and clear pathogens: key mechanisms of action: Increasing vascular permeability and chemotaxis: destroying pathogen cell membranes. Increasing recognition of pathogens and facilitating phagocytosis (opsonization) Initially, components are inactive pro-proteases (aka zymogens: activated in 3 ways, classical pathway, alternative pathway, lectin pathway, acting as a cascade, proteolytic cleavage generating two fragments:
