classic complement pathway
classic complement pathway
Immunology The usual route of activation of the complement cascade, initiated by C1q binding to either IgM or to 2 adjacent IgG molecules; the resulting conformational change of C1q autoactivates C1r2, in turn activating C1s2, cleaving C4–C4b followed by C2–C2a; C4b,2a–the C3 convertase of CCP–initiates opsonization, leukocyte chemotaxis, ↑ vascular permeability, and cytolysis; CCP is activated by IgG, IgM, DNA, staphylococcal protein A and C-reactive protein; both classic and alternate pathways are stimulated by trypsin-like enzymes. See Common pathway. Cf Alternate pathway. McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.
References in periodicals archive
Low CH50 was suggestive of
classic complement pathway deficiency, but any specific cause for it could not be elucidated.
In patients with immune complex type MPGN, the paraprotein likely forms part of the immune complex causing activation of the
classic complement pathway and resulting in renal injury with both abnormal immunoglobulin and complement on immunohistochemistry.
Markham et al suggest transient glomerular deposition and clearance of small amounts of immune complexes formed during natural antibody response mechanisms in vivo, which initiates the
classic complement pathway resulting in generation and deposition of C4d.
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