Integrin alpha-M beta-2 (Macrophage-1 antigen, complement receptor 3) (CD11b/CD18)

Integrin alpha-M beta‑2—commonly known as CD11b/CD18, Macrophage‑1 antigen, Mac‑1, or complement receptor 3 (CR3)—is a heterodimeric β₂ integrin composed of the CD11b (αM) subunit encoded by ITGAM and the CD18 (β₂) subunit encoded by ITGB2[1][7]. It is predominantly expressed on polymorphonuclear leukocytes, monocytes/macrophages, dendritic cells, NK cells, subsets of T cells, and B cells. This integrin mediates key immune processes including cellular adhesion to endothelium via ligands like ICAM‑1 and fibrinogen; phagocytosis through recognition of iC3b-opsonized targets; chemotaxis toward inflammatory signals; respiratory burst activity in neutrophils; and resolution of inflammation. CD11b/CD18 plays central roles in both innate immunity—by facilitating pathogen clearance—and pathological conditions such as chronic inflammation, cardiovascular diseases like hypertension/atherosclerosis,[4] cancer progression,[2] infection susceptibility,[7] and therapy resistance/minimal residual disease in leukemia.[5] Pharmacological targeting has focused on monoclonal antibodies that block ligand binding or modulate activation state. While preclinical models show benefit from inhibiting this pathway—for example reducing tissue injury after ischemia or enhancing tumor response to radiotherapy—clinical translation has been challenging due to limited efficacy despite favorable safety profiles.[2] CD11b expression serves as an important biomarker for risk stratification in certain hematologic malignancies.[5] Safety concerns include possible impairment of host defense mechanisms due to broad suppression of myeloid cell functions. Overall, integrin alpha-M beta‑2 remains an important therapeutic target under investigation for its multifaceted role at the interface between immunity, inflammation, vascular biology, infection control, cancer biology—and clinical outcomes across these domains.[1][7][8]

Other names

Macrophage-1 antigenIntegrin αMβ2Mac-1Complement receptor 3 (CR3)

Blockade of integrin-mediated cell adhesion and migration by antibody binding to CD11b/CD18, reducing leukocyte recruitment and inflammatory responses Agonist-induced activation or inhibition modulates downstream signaling pathways involved in immune cell function and vascular remodeling