“…Moreover, CD40 ligation induces expression of adhesion molecules such as CD54, CD62E, and CD106 on endothelial cells, suggesting that CD40 signaling plays an important role in leukocyte extravasation to sites of inflammation (5,6). In recent years, greater attention has been paid to the role of CD40-CD40L interactions in the immunopathogenesis of some autoimmune diseases, where T or B cells have a prominent role, such as systemic lupus erythematosus (7), rheumatoid arthritis (8), and multiple sclerosis (9) as well as in allograft rejection (10). Administration of mAb directed against CD40L has been shown to effectively inhibit inflammatory responses in a variety of animal models such as experimental allergic encephalomyelitis (9,11), lupus nephritis (12), collagen-induced arthritis (13), atherosclerosis (14), and spontaneous autoimmune diabetes (15).…”