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Complement receptor type 1 (CD35), also known as CR1, is a large transmembrane glycoprotein that serves as a critical regulator of the complement system [UniProt: P17927]. It is expressed on various cell types, including erythrocytes, B cells, neutrophils, and follicular dendritic cells (FDCs) within the germinal centers of lymphoid organs [NCBI Gene: 1378]. On FDCs, CD35 is essential for capturing and retaining opsonized antigens in the form of immune complexes, which are then presented to B cells to facilitate the germinal center reaction and antibody affinity maturation [PubMed: 16455988]. CD35 functions by binding to C3b and C4b fragments, acting as a cofactor for Factor I-mediated degradation and accelerating the decay of C3 and C5 convertases, thereby preventing excessive complement activation [PubMed: 19302238]. In clinical contexts, CD35 is implicated in the pathogenesis of systemic lupus erythematosus (SLE), where reduced erythrocyte expression leads to impaired immune complex clearance, and in Alzheimer's disease, where it is linked to amyloid-beta clearance [PubMed: 25607777, PubMed: 19838190]. Therapeutic strategies targeting CD35 often involve the use of soluble CR1 derivatives to inhibit complement-mediated tissue injury in conditions like ischemia-reperfusion injury and organ transplantation [PubMed: 11544344].
Inhibition of C3 and C5 convertases; cofactor for Factor I-mediated cleavage of C3b and C4b
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