Complement activation and vascular injury in systemic lupus erythematosus.
The deposition of immune complexes within blood vessel walls results in the potential for complement activation and the release of chemotactic factors, such as fragments of C5 (C5fr). The generation of C5fr results in the intravascular aggregation of neutrophils with subsequent leukostatic occlusion of the pulmonary arterioles. The generation of C5fr may contribute to the pathogenesis of adult respiratory distress syndrome and other diseases. Studies were undertaken to determine the role of circulating complement derived peptides and intravascular neutrophil activation in systemic lupus erythematosus.
D000936:Antigen-Antibody Complex / Q000276:immunology; D003167:Complement Activation; D003176:Complement C3 / Q000031:analogs & derivatives / Q000502:physiology; D015926:Complement C3a / Q000031:analogs & derivatives*; D003182:Complement C5 / Q000031:analogs & derivatives / Q000502:physiology; D015937:Complement C5a, des-Arginine; D006801:Humans; D007105:Immune Complex Diseases / Q000276:immunology*; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D010488:Polyarteritis Nodosa / Q000276:immunology*
D000936:Antigen-Antibody Complex; D003176:Complement C3; D003182:Complement C5; D015937:Complement C5a, des-Arginine; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a