Complement activation is the triggered, sequential operation of the complement system, a network of plasma and cell-surface proteins that forms a central effector arm of innate immunity. Activation proceeds through three converging routes, the classical, lectin, and alternative pathways, which differ in their initia…
Complement activation is the triggered, sequential operation of the complement system, a network of plasma and cell-surface proteins that forms a central effector arm of innate immunity. Activation proceeds through three converging routes, the classical, lectin, and alternative pathways, which differ in their initiating recognition events: antibody-antigen complexes, the binding of mannose-binding lectin and related molecules to microbial carbohydrates, and the spontaneous, surface-regulated turnover of complement components. Each pathway converges on the cleavage of central components, generating opsonins that tag pathogens for phagocytosis, anaphylatoxins that promote inflammation and recruit immune cells, and the membrane attack complex that lyses susceptible targets. Tight regulation by inhibitory proteins normally restricts complement to appropriate surfaces, and dysregulated or excessive activation contributes to tissue injury and inflammatory and autoimmune disease, including the inflammatory processes implicated in arthritic joints and in severe infection. Lectin-pathway recognition of carbohydrate structures also links complement to host defense against viruses. The significance of complement activation spans infection, inflammation, autoimmunity, and immunopathology, informing both diagnosis and therapy. Sub-areas include the classical, lectin, and alternative pathways, opsonization, anaphylatoxin signaling, the membrane attack complex, complement regulation, and the role of complement in inflammatory and immune-mediated disease.
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