Integrin alpha L (CD11a) (CD11a)

Integrin alpha L (CD11a) is the alpha subunit of the heterodimeric integrin Lymphocyte Function-associated Antigen-1 (LFA-1), which also comprises the CD18 (beta 2) subunit. Expressed exclusively on leukocytes, CD11a is a critical mediator of the immune response, facilitating cell-to-cell adhesion by binding to Intercellular Adhesion Molecules (ICAMs) on endothelial cells and antigen-presenting cells [7, 16, 20]. This interaction is essential for the extravasation of leukocytes from the bloodstream into inflamed tissues and the formation of the immunological synapse, which drives T cell activation and proliferation [6, 15, 21]. Dysregulation of CD11a-mediated pathways is central to the pathogenesis of various inflammatory and autoimmune conditions, including chronic plaque psoriasis and dry eye disease, as well as the rejection of transplanted organs [9, 12, 13]. Therapeutic strategies targeting CD11a include monoclonal antibodies like efalizumab and small molecule antagonists like lifitegrast, which competitively block the LFA-1/ICAM-1 interface to suppress pathological inflammation [8, 11, 14]. While effective, systemic inhibition of CD11a has been linked to severe safety risks, most notably the development of progressive multifocal leukoencephalopathy (PML), which led to the market withdrawal of efalizumab [1, 4, 5].

Other names

ITGALCD11ALFA-1 alphaIntegrin subunit alpha LLeukocyte adhesion glycoprotein LFA-1 alpha chainLymphocyte function-associated antigen 1 alpha polypeptideLeukocyte function-associated molecule 1 alpha chain

Inhibition of the interaction between the LFA-1 (CD11a/CD18) complex and its ligands, such as Intercellular Adhesion Molecule-1 (ICAM-1), which prevents leukocyte adhesion, extravasation, and the formation of the immunological synapse required for T cell activation.