Immune phenomena are believed to play a key role in the pathogenesis of tissue damage in Crohn’s disease and ulcerative colitis.1 ,2 Although some of the immunological perturbations seem to be shared by Crohn’s disease and ulcerative colitis, there are important distinguishing features, possibly reflecting different pathways of immune mediated intestinal inflammation. Evidence indicates that macrophage and T cell derived cytokines play a key role in the amplification and perpetuation of the inflammatory response in both disorders.3 No aberrant cytokine secretion has been documented in inflammatory bowel disease (IBD) and no convincing evidence has as yet been provided that cytokine changes occur as a result of disease specific immune activation. However, a number of quantitative changes in the secretion and/or activity of both proinflammatory and regulatory cytokines have been reported in Crohn’s disease and ulcerative colitis. Based on variation in the magnitude of these changes there seem to be different cytokine profiles into which the inflammatory process may fall during the course of the disease. Studies from murine models indicate that two T lymphocyte subsets may be defined depending on their cytokine secretion profiles: Th1 lymphocytes producing interleukin (IL) 2 and interferon γ (IFN-γ), and Th2 lymphocytes producing IL-4, IL-5 and IL-10. When taken together all available data from both …