ITGAM

ITGAM Full Name

integrin alpha M

ITGAM Introduction

ITGAM, also known as integrin alpha M or CD11b, encodes a key cell surface receptor widely expressed on myeloid lineage cells, including monocytes, macrophages, and microglia. As part of the integrin family, ITGAM forms the Mac-1 complex (CD11b/CD18), which mediates cell adhesion, migration, and immune signaling. Clinically, ITGAM has gained attention not only as a regulator of innate immune responses but also as a potential biomarker and therapeutic target in conditions where inflammation, tissue remodeling, and immune surveillance are critical. Its broad functional repertoire links vascular, autoimmune, and neurological disorders, highlighting its relevance for patients who struggle with chronic inflammation or injury-related immune dysfunction.

Functionally, ITGAM/CD11b orchestrates multiple immune processes, including phagocytosis, leukocyte adhesion to the endothelium, and modulation of inflammatory signaling pathways. It interacts with Toll-like receptors, Akt signaling, and other immune mediators to fine-tune cytokine secretion and cell migration. Dysregulation of ITGAM can exacerbate tissue injury by amplifying inflammatory responses or impairing debris clearance. Conversely, activation or targeted modulation of ITGAM has protective effects in disease models, such as suppressing TLR7-driven inflammation in lupus nephritis or enhancing debris clearance after optic nerve injury, demonstrating that ITGAM is a versatile node in the immune network with both diagnostic and therapeutic potential.

Disease-focused studies underscore ITGAM's significance across autoimmune, vascular, and neurological conditions. In systemic lupus erythematosus, ITGAM activation reduces kidney inflammation and prevents disease progression, suggesting a novel therapeutic avenue. In abdominal aortic aneurysm, ITGAM deficiency attenuates vascular remodeling and inflammatory cytokine expression, revealing its role in vascular integrity. In ischemic stroke, elevated ITGAM expression correlates with worse outcomes, positioning it as a potential biomarker and therapeutic target. Moreover, in optic nerve injury, ITGAM deletion in microglia enhances axonal debris clearance via IGF-1, promoting tissue repair. Collectively, these findings highlight ITGAM as a critical immune regulator and an actionable target for inflammation-driven diseases, offering hope for improved diagnostics and targeted interventions.

Alternate Names for ITGAM

ITGAM; integrin alpha M; CR3; CR3A; MAC1; Cd11b; Ly-40; Mac-1; Mac-1a; CD11b/CD18

• 1.Li X, et al.; CD11b suppresses TLR7-driven inflammatory signaling to protect against lupus nephritis. bioRxiv [Preprint]. 2024.26.605143.
  2.Zhou M, et al.; Deficiency of ITGAM Attenuates Experimental Abdominal Aortic Aneurysm in Mice. J Am Heart Assoc. 2021, 10(7):e019900.