Infliximab (RemicadeTM) in uveitis: a review

umor necrosis factor (TNF)-α has been implicated as an important mediator in autoimmune ocular inflammatory disease pathogenesis as shown by animal studies and its detection in the ocular fluids of patients with uveitis. Blockade of TNF-α has emerged as one of the most promising therapies in autoimmune diseases including uveitis. Currently, there are three TNF-α antagonists: two monoclonal antibodies (infliximab and adalimumab) and a soluble receptor that binds soluble TNF-α (etanercept). Infliximab is a chimeric monoclonal antibody directed against TNF-α. It binds with high affinity to both the soluble and the membrane-bound TNF-α and inhibits a broad range of biologic activities of TNF-α. Binding to membrane TNF-α can mediate programmed cell death. Several studies reported that infliximab therapy was rapidly effective and safe treatment for refractory noninfectious uveitis including childhood uveitis and is indicated as rescue therapy for relapses of ocular inflammation or as maintenance therapy when conventional immunosuppression fails. It also allowed a reduction of corticosteroids and immunosuppressive drugs required to control the disease. However, repeated infusions are required to maintain long-term remission. Moreover, infliximab administration is costly and requires hospital admission. Adalimumab, fully humanized monoclonal anti- TNF-α antibody, was also found to be effective and safe therapy for the management of refractory noninfectious uveitis. Several studies reported that infliximab was more effective than etanercept in the treatment of refractory uveitis. Perhaps infliximab’s ability to target membrane-bound TNF-α in addition to the soluble form may contribute to its increased efficacy in comparison with etanercept for uveitis.