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The classical complement pathway is one of three major pathways (alongside lectin and alternative pathways) that activate the complement system—a central component of immune surveillance and host defense. It is initiated by binding of antigen–antibody complexes (chiefly involving IgG or IgM antibodies) to the C1 complex, composed of C1q, C1r, and C1s. Activation triggers a cascade of proteolytic events leading to the formation of the classical pathway C3 convertase (C4b2b), subsequent cleavage of C3 and C5, and ultimately the formation of the membrane attack complex (MAC), resulting in lysis of target cells. Specific component deficiencies, autoantibodies (nephritic factors), or genetic mutations can cause or contribute to disease states, including SLE and glomerulonephritis. Therapeutic reduction of the classical pathway is a proposed or active treatment strategy for conditions linked to excessive or inappropriate complement activation.
Inhibition of complement activation (by blocking activation of C1 or downstream components); Reduction of inflammatory and immune damage mediated by complement cascade
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