Complement activation is the sequential, enzyme-driven triggering of the complement system, a network of plasma and membrane proteins that forms a central arm of innate immunity and bridges to adaptive responses. Activation proceeds through three converging routes: the classical pathway, initiated when C1q binds ant…
Complement activation is the sequential, enzyme-driven triggering of the complement system, a network of plasma and membrane proteins that forms a central arm of innate immunity and bridges to adaptive responses. Activation proceeds through three converging routes: the classical pathway, initiated when C1q binds antibody-antigen complexes; the lectin pathway, triggered when mannose-binding lectin and ficolins recognise microbial carbohydrate patterns; and the alternative pathway, which amplifies through spontaneous C3 turnover on permissive surfaces. All three generate C3 and C5 convertases, cleaving C3 and C5 to produce opsonins such as C3b that tag pathogens for phagocytosis, anaphylatoxins C3a and C5a that recruit and activate inflammatory cells, and the terminal C5b-9 membrane attack complex that lyses susceptible targets. Beyond defence against microbes, complement clears immune complexes and apoptotic debris, modulates B- and T-cell responses, and contributes to tissue homeostasis. Tight regulation by inhibitory proteins prevents host injury, and dysregulated or excessive activation contributes to autoimmune, inflammatory, ischaemic, and infectious tissue damage. Quantification of complement components and split products serves as a marker of immune activity and disease, and the cascade is an active therapeutic target. Research addresses pathway regulation, biomarkers, and complement-directed intervention.
5 peer-reviewed articles, ranked by relevance. Each links to its DOI.
The 5 articles above have been cited 17 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.
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