Integrin alpha M (CD11b) (ITGAM)

Integrin alpha M (CD11b), frequently identified in rodent research via the OX42 monoclonal antibody, is a critical component of the Mac-1 (CD11b/CD18) heterodimeric integrin receptor (Robinson et al., 1986). This molecule is primarily expressed on myeloid-lineage cells, including microglia, macrophages, and neutrophils, where it facilitates cell-cell and cell-matrix interactions (UniProt P11215). The term OX42-positive microglia refers to the activated state of these cells, characterized by the upregulation of CD11b during neuroinflammatory processes (Schmid et al., 2018). CD11b plays a pivotal role in the innate immune system by mediating leukocyte adhesion, transendothelial migration, and the phagocytosis of complement-opsonized pathogens or debris (NCBI Gene: 3684). In various neurodegenerative and inflammatory diseases, such as Alzheimer's disease and stroke, the persistent activation of CD11b-expressing microglia contributes to tissue damage and disease progression. Therapeutic strategies targeting CD11b involve small molecule modulators, such as Leukadherin-1, which aim to stabilize the integrin in specific conformational states to reduce harmful inflammation while maintaining protective immune functions (Schmid et al., 2018). Overall, CD11b serves as both a vital marker for microglial activation and a promising therapeutic target for controlling myeloid-driven pathology.

Other names

CD11bITGAMMac-1 alpha subunitComplement receptor 3 alphaOX-42 antigenCR3AMO1A

Allosteric modulation of the Integrin alpha M subunit to regulate myeloid cell adhesion, migration, and phagocytic activity (Schmid et al., 2018).