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classic complement pathway

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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.


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In a pneumococcus-naive host (or in the absence of antibody to pneumococcal capsule) host-cell phagocytosis is severely limited because of the inhibition of phagocytosis and the inhibition of the activation of the classic complement pathway.
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.
On one hand, it seems to have pro-inflammatory effects, such as activating the classic complement pathway and decreasing IL-6 receptor concentrations in areas where IL-6 has anti-inflammatory effects.
 
 
 
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