Several immunological alterations have been described in inflammatory bowel disease, but their role in the pathogenesis of tissue damage of these disorders is not fully known. Activated immune cells produce proinflammatory and regulatory cytokines able to mediate immune mechanisms underlying intestinal inflammation in both ulcerative colitis and Crohn's disease. Although there is no evidence for an aberrant cytokine secretion in the intestinal mucosa of patients with inflammatory bowel disease, observations seem to indicate that locally released cytokines trigger the preferential differentiation of mucosal lymphocytes into TH1 or TH2 subsets. The unresponsiveness of intestinal mononuclear cells to the inhibiting effects of regulatory cytokines may, also, contribute to this differentiation.