Activation of the human terminal complement pathway in atherosclerosis.
The presence of the terminal C5b-9 complement complex in tissues indicates that complement activation has occurred in situ with subsequent membrane damage, tissue injury, and inflammatory response mediation. The terminal C5b-9 neoantigens of the complement system, S protein C3c, C3d, and apolipoprotein B deposits were localized in 20 aortic fibrous plaques, 12 aortic intimal thickenings, 8 aortic fatty streak intimae, 14 coronary fibrous plaques, 5 coronary intimal thickenings, and 8 femoral fibrous plaques, using an indirect and double-staining immunoperoxidase technique. The specific granular deposits were present from the early to the advanced stages of atherosclerosis in relation to the degree of fibrosis and necrosis. The different double-staining localization of C5b-9 and S protein may suggest local assembly of the complex as a consequence of complement activation and may sustain its role in the chronic progression of atherosclerosis.
D001011:Aorta / Q000032:analysis / Q000473:pathology; D001055:Apolipoproteins B / Q000032:analysis; D001161:Arteriosclerosis / Q000276:immunology* / Q000473:pathology; D003167:Complement Activation; D015938:Complement Membrane Attack Complex; D003165:Complement System Proteins / Q000032:analysis; D003331:Coronary Vessels / Q000032:analysis / Q000473:pathology; D005260:Female; D005263:Femoral Artery / Q000032:analysis / Q000473:pathology; D005355:Fibrosis; D006023:Glycoproteins / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D019096:Vitronectin
D001055:Apolipoproteins B; D015938:Complement Membrane Attack Complex; D006023:Glycoproteins; D019096:Vitronectin; D003165:Complement System Proteins