Mouse Intercellular Adhesion Molecule-1 (ICAM-1, CD54) is a transmembrane glycoprotein belonging to the immunoglobulin superfamily that plays a central role in leukocyte adhesion, immune synapse formation, and inflammatory cell trafficking in mice (Mus musculus). ICAM-1 is constitutively expressed at low levels on endothelial cells, epithelial cells, and certain immune cells, and is strongly upregulated in response to pro-inflammatory cytokines such as TNF-α, IL-1β, and IFN-γ. It binds to β2 integrins, including LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18), on leukocytes to mediate firm adhesion to the endothelium and subsequent transmigration into inflamed tissues. Murine ICAM-1 is critically involved in widely used experimental models of inflammatory and autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE), collagen-induced arthritis, inflammatory bowel disease, asthma, sepsis, and transplant rejection. ICAM-1–deficient (knockout) mouse models have been instrumental in defining its role in leukocyte recruitment, T-cell activation, and tissue injury. As both a functional mediator and biomarker of inflammation, mouse ICAM-1 is extensively utilized in immunology, vascular biology, oncology, and infectious disease research to investigate mechanisms of immune cell trafficking and to evaluate anti-inflammatory and immunomodulatory therapeutic strategies.