Intercellular adhesion molecule 1 and Integrin alpha L (ICAM-1/CD11a)

The interaction between Intercellular Adhesion Molecule 1 (ICAM-1, also known as CD54) and Integrin alpha L (CD11a, a component of the LFA-1 complex) is a central event in the immune response, facilitating leukocyte trafficking and the stabilization of the immunological synapse (UniProt P05362; UniProt P20333). On dendritic cells, ICAM-1 acts as a critical ligand for LFA-1 on T cells, a process essential for efficient antigen presentation and T-cell activation (PubMed PMID 15634887). Conversely, CD11a on dendritic cells can participate in their migration and interaction with other immune cells (PubMed PMID 11169396). This molecular interaction is a major therapeutic target for inflammatory and autoimmune conditions, as its blockade can inhibit the recruitment and activation of pathogenic T cells. Drugs such as lifitegrast and efalizumab have been developed to disrupt this pathway by binding to the CD11a subunit, thereby preventing its association with ICAM-1 (Xiidra FDA Label; PubMed PMID 14647403). While effective in treating conditions like dry eye disease and psoriasis, systemic inhibition of this pathway has been linked to serious safety concerns, including an increased risk of opportunistic infections and progressive multifocal leukoencephalopathy (FDA).

Other names

CD54ITGALLFA-1 alpha subunitICAM-1/LFA-1 interactionAntigen CD11A (p180), lymphocyte function-associated antigen 1; alpha polypeptideMajor group rhinovirus receptor

Inhibition of the interaction between ICAM-1 and the LFA-1 (CD11a/CD18) complex, which prevents leukocyte adhesion to the endothelium and the formation of the immunological synapse between T cells and antigen-presenting cells (PubMed PMID 14647403; Xiidra FDA Label).