Main Article Content
Tumor necrosis factor-alpha (TNF-α) is an inflammatory cytokine that is important in the inflammatory process and apoptotic cell death. TNF- α plays a significant role in the pathogenesis of rheumatoid arthritis and Crohn' s disease. Therefore, anti-TNF-α therapy has been introduced to clinical use to delay the progress of these diseases. This article discusses the properties of anti-TNF-α. antibody (infliximab), a chimeric mouse/human monoclonal antibody. Inhibition of TNF-α. showed benefits to rheumatoid arthritis patients by 1) reduction of local and systemic proinflammatory cytokines; 2) reduction of lymphocyte migration to the joints and decrease of macrophage and T-cell interaction; 3) reduction of angiogenesis around the joints. Altogether, these effects improve clinical symptoms. In Crohn's disease, the chimeric anti-TNF-α. antibody decreases C-reactive protein (an inflammatory marker). Additionally, the biopsy of intestinal mucosa from patients show diminished number of cells that produce TNF-α and interferon-α. Moreover, the chimeric anti-TNF- α antibody inhibited migration of inflammatory cells to the pathologic region of intestine, and attenuated inflammatory marker in this area. In several clinical trials, infliximab or infliximab plus methotrexate have been found to be efficacious and well tolerated in the treatment of rheumatoids arthritis and Crohn's disease.
Upon acceptance of an article, the Pharmacological and Therapeutic Society of Thailand will have exclusive right to publish and distribute the article in all forms and media and grant rights to others. Authors have rights to use and share their own published articles.