Complement receptor type 3 (CR3 (also known as Mac-1, integrin αMβ2, or CD11b/CD18))

Complement receptor type 3 is a heterodimeric integrin receptor (also known as Mac-1, CD11b/CD18, and integrin αMβ2) highly expressed on myeloid leukocytes such as macrophages, neutrophils, and dendritic cells[3][4][2]. It recognizes iC3b, a cleaved fragment of complement component C3 deposited on opsonized particles, microorganisms, or apoptotic cells[5][1][4]. This recognition triggers phagocytosis and helps clear pathogens and cell debris, playing an essential role in innate and adaptive immunity via antigen handover to CR2-expressing cells such as B lymphocytes[1][2][3]. CR3 is also a promiscuous receptor, binding various other ligands including fibrinogen, denatured proteins, DAMPs, and dsRNA, contributing to roles in homeostasis and inflammation[4][3]. It is a critical immune effector and significant drug target in contexts of infection, inflammation, and autoimmunity[4][3][5].

Other names

Mac-1integrin αMβ2CD11b/CD18integrin alpha-Mcomplement receptor 3

Blockade of receptor-ligand interaction (e.g., anti-CD11b antibodies prevent opsonophagocytosis). Modulation of macrophage phenotype (e.g., through CR3 engagement). Inhibition of complement cascade reduces CR3-dependent cell activation and phagocytosis.