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23 Cards in this Set
- Front
- Back
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complement system is an essential part of
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the innate immune system
enhances phagocytosis and removal of Ag from circulation and from tissues (opsonization, C3b) |
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complement fragments cause
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vasodilation: C2a, C4a, C3a, C5a
direct accumulation of pmn's to Ag in tissue: chemotaxis, C3a, C5a lysis of bacteria and virus infected cells: membrane attack complex, C5-C9 |
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how many protein in complement system
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group of 9 major proteins that normally circulate in blood in an inactive form: zymogens or proenzymes
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complement may be activated by
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Ab-Ag interaction: classical pathway
by contact with certain bacteria, viruses and fungi either through: - alternate pathway - lectin mammose pathway |
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overview of complement system
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innate immunity
9 major proteins (produced by liver) - C1-C9 blood and tissue as zymogens cascade: series of rxns catalyzed by enzymes that are activated sequentially by products of previous rxn intermediates have major impact |
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complement intermediates impact
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Ag removal immune complexes: opsonization
lytic cycle - membrane attack complex vasodilation and neutrophil chemotaxis/activation (PMNs) |
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activation process of complement is
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deliverate
targeted controlled |
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activation process: deliberate
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Classical: Ag-Ab complex bind C1 and fits in 2 Fc regions = activate C1 enzyme
this cleaves C4, which forms C2 - C14b2a C3 convertase splits C3 ino C3a + C3b - if in circulation: Ab-Ag cleared by fixed phagocytic system - if in tissue: Ag-Ab cleared by C3 + C5a: potent chemotactic factors for PMN's = bring system to bug; vasodilate and adherance factors C6-C9: lytic component; perforin holes and lysis (membrane attack complex) feedback loop/takeover path: when C3b on PM cause factor D, B, and properdin: forms new 3 convertase |
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activation prcoess: targeted
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lectin mannose pathway
= same as classic pathway, EXCEPT: no Ab near C2+C4: convertase activated directly by look alike lectin (C1) makes M14b2a complex instead |
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activation process: controlled
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alternative pathway: feed back loop and lytic path
- in tissue: C3 is high and hydrolyzes to C3a and C3b, which is turned over and enzymes get rid of it - if pathogen present, C3b sticks on PM and activates loop and lysis |
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hereditary angioedema
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mutation in C1 inhibitor due to stress hormones/anxiety
automatically activates pathway and generates C3a and C5a life threatening give pt C1 inhibitor |
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biological effects of complement
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processing immune complexes:
-circulation: IC in circ -opsonization Ag clearance -fixed phagocytic system -kupffer cells in livver -splenic mac in spleen -mesangial ma in kidney RBC transport of circulating IC's to "fixed phagocytes memory B cell generation anaphylatoxins |
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RBC transport of circulating IC's to fixed phagocytes by
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low affinity CR1 R's for a fragment of C3 (C3c)
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anaphylatoxins are potent inducers of
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inflammation
tissue: IC in tissue - C3b: opsonization; C3b R's on phagocytic cells - C3a, C5a: chemotaxis |
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C3a and C5a effects
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vasodilation
adhesion PMN chemotaxis phagocytes gradient migration activation phagocytes |
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Role of C3 in processing of IC's
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reduction in lattice size
binding to erythrocyte CR1 and transport to mononuclear phagocyte system uptake by fixed mononuclear cells and degradation of Ag localization to B cell, follicular dendritic cell and APC's |
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role of complement in inflammation
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IC clearance
mast cell degranulation opsonization lysis chemotaxis brings PMN's |
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the beneficial effects of complement activation in supporting innate and acquired immune responses against infectious diseases can also cause disease or create complications of a primary disease by
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over activation
continual activation activation in wrong place |
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complement in pathogenesis of disease can result in
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system shock
organ/tissue destruction chronic inflammation Ab initiatied; complement amplified associated with Type II and III hypersensitivity |
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complement may cause disease pathogenesis by
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systemic production of anaphylatoxins
- following grame negative sepsis insertion of membrane attack kcomplex into host cells leading to cellular activation and stimulation of membrane arachidonic acid metabolism fixation of C3 to IC's localized in tissues causing recruitment and activation of tissue and circulating leukocytes |
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C5a in pathogenesis causes
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systemic complement activation
- shock, lung and vascular collapse |
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membrane attack complex in pathogenesis
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tissue necosis
prostaglandins and leukotrienes cell activation |
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C3b in pathogenesis
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IC in tissues
neutrophil + monocyte activation |
