Abstract
In recent years, new concepts have been formulated for the pathogenesis and therapeutic management of ulcerative colitis (UC) and Crohn's disease (CD) . In the inflamed intestinal mucosa, analysis of the types of immune response ongoing has revealed that there is predominantly a T-helper cell type 1 response in CD, with exaggerated production of IL-12 and IFN-γ, whereas the lesion seems more of an antibody-mediated hypersensitivity reaction in UC. Despite these differences, downstream inflammatory events could be similar in both conditions. IL-1β, IL-6, IL-8 and TNF-α are produced in excess in both UC and CD. New medical therapies that inhibit the bioactivity of TNF-α represent a major breakthrough in the treatment of CD. The mouse chimeric monoclonal antibody infliximab against TNF-α is effective for treating active CD, closing fistulas, and maintaining remission. Side effects occurring in CD patients treated with infliximab include human anti-chimeric antibodies, worsening infections, or malignancies of unknown relationships. This review seeks to summarize analysis about manipulation of cytokines especially focusing into TNF-α in inflammatory bowel diseases and studies in which anti TNF-α antibody has been used in the treatment of CD.