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Pathologic Effects of the Complement System

المؤلف:  Abbas, A. K., Lichtman, A. H., Pillai, S., & Henrickson, S. E.

المصدر:  Cellular and Molecular Immunology (2026)

الجزء والصفحة:  11E, P316

2026-09-27

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Even when it is properly regulated and appropriately activated, the complement system can cause significant tissue damage. Some of the pathologic effects associated with bacterial infections may be due to complement-mediated acute inflammatory responses to infectious organisms. In some situations, complement activation is associated with intravascular thrombosis and can lead to ischemic injury to tissues. For instance, antiendothelial antibodies against vascularized organ transplants and the immune complexes produced in autoimmune diseases may bind to vascular endothelium and activate complement, thereby leading to inflammation and generation of the MAC with dam age to the endothelial surface, which favors coagulation. There is also evidence that some of the late complement proteins may activate prothrombinases in the circulation that initiate thrombosis independent of MAC-mediated damage to endothelium.

The clearest examples of complement-mediated pathology are immune complex–mediated diseases. Systemic vasculitis and immune complex glomerulonephritis result from the deposition of antigen-antibody complexes in the walls of blood vessels and kidney glomeruli. Complement activated by these deposited immune complexes initiates the acute inflammatory responses that destroy the vessel walls or glomeruli and lead to thrombosis, ischemic damage to tissues, and scarring. Studies with knockout mice lacking the complement proteins C3 or C4 or lacking Fcγ receptors suggest that Fc receptor–mediated leukocyte activation may also cause inflammation and tissue injury as a result of IgG deposition, even in the absence of complement activation.