Role of Gene Polymorphism of Intercellular Adhesion Molecule 1 (ICAM 1) in Rheumatoid Arthritis

Abstract

Joint and extra-articular inflammation are hallmarks of rheumatoid arthritis (RA) that is a systemic autoimmune disease. This condition is long-lasting and mostly affects the synovial joints. Untreated, it spreads from its initial presentation in minor peripheral joints to larger proximal joints. Cartilage and bone deterioration occur as a result of chronic inflammation in a joint. Early RA is diagnosed when symptoms have been present for less than six months, while established RA is diagnosed when symptoms have been present for more than six months. A transmembrane protein belonging to the immunoglobulin superfamily, intercellular adhesion molecule 1 (ICAM-1) is expressed on the surface of several cell types and is stimulated by inflammatory stimuli. By binding to the two integrins, leukocyte function-associated antigen 1 and macrophage antigen 1, as well as other ligands, it mediates cellular sticky connections. Numerous of these molecules are crucial to the rheumatoid arthritis disease process. ICAM-1 gene polymorphism and rheumatoid arthritis clinical activity are related, and a variety of drugs can be used to treat RA by reducing ICAM-1 expression.