Complement receptor 3 and complement pathway components (CR3/Complement)

The complement system is a complex network of over 30 plasma and cell-surface proteins that serve as a primary mediator of the innate immune response (Ricklin et al., 2010). Complement receptor 3 (CR3), also known as Mac-1 or integrin alpha-M beta-2 (CD11b/CD18), is a key myeloid receptor that recognizes iC3b-opsonized targets to facilitate phagocytosis and leukocyte recruitment (UniProt P11215). The broader complement pathway involves a proteolytic cascade—comprising the classical, lectin, and alternative pathways—leading to the activation of C3 and C5, which drive inflammation and the formation of the membrane attack complex (Janeway's Immunobiology). Dysregulation of these components is central to the pathogenesis of diseases such as paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome (aHUS), and various neurodegenerative conditions where CR3 mediates aberrant synaptic pruning (Hong et al., 2016). Therapeutic strategies include the use of monoclonal antibodies like eculizumab (targeting C5) and small molecules or peptides like pegcetacoplan (targeting C3) to prevent overactivation (FDA, 2021). Targeting CR3 and specific pathway components remains a critical area of drug development for managing complement-mediated tissue damage and chronic inflammation (Mastellos et al., 2019).

Other names

CR3Mac-1Integrin alpha-M beta-2CD11b/CD18Complement systemComplement cascade

Inhibition of C5 cleavage, C3 inhibition, Factor B inhibition, Factor D inhibition, C1s inhibition, and C5a receptor antagonism.