ITGAM
Integrin subunit alpha M (CD11b / CR3)
Also known as: ITGAM, CD11b, CR3, Mac-1
Biology & Mechanism
ITGAM encodes the CD11b subunit of the complement receptor CR3 (Mac-1), which mediates phagocytosis of C3b-opsonized substrates including synapses and amyloid. Variants at the ITGAM locus are associated with Alzheimer's disease risk. CR3 on microglia mediates complement-dependent synaptic pruning; excessive CR3-mediated pruning may contribute to synapse loss in neurodegeneration. ITGAM expression is upregulated in activated microglia.
Open Questions
- —Can selective blockade of CR3-mediated synaptic pruning be achieved without broadly impairing complement-dependent phagocytosis?
- —What is the relative contribution of CR3 versus TREM2 to amyloid phagocytosis by microglia?
- —Does ITGAM risk variant alter CR3 expression or function in human microglia?
Sources
- The complement system in neurological diseases (2018)
Last reviewed: June 1, 2026