Abstract
Activation of complement component C1 composed of C1q, C1r, and C1s initiates the classical complement pathway. This occurs by binding of C1q to immune complexes (ICs), apoptotic bodies, or pathogens, leading to autocatalytic activation of C1r and subsequent cleavage of the zymogen C1s. The classical complement pathway is involved in pathogen recognition, antibody-mediated cytotoxicity, and clearance of ICs and apoptotic debris.1 Rare monogenic deficiencies in any of the C1 complement components are strongly linked to systemic lupus erythematosus (SLE).
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