IL-2 is an indispensable regulatory cytokine of the immune system that has multiple functions, including the activation of T cells, macrophages, lymphokineactivated killer (LAK) cells, and natural killer (NK) cells; the differentiation of B cells; and activation-induced cell death (AICD). In 1993, Sadlack3 reported that, in mice with a disrupted IL-2 gene, approximately 50% would die at between 4 and 9 weeks of age with splenomegaly, lymphadenopathy, and autoimmune hemolytic anemia and that chronic colitis would occur in the rest at between 6 and 15 weeks. The small intestine of this model is intact, whereas the colon (from rectum to cecum) is severely affected with ulcers and wall thickening. Pathologically, crypt abscesses, mucin depletion, and dysplasia of the epithelial cells (which are the features of human IBD) were observed. Infiltration of activated T cells and B cells; increases in IgG1, IgE, and anticolon antibodies; and increased expression of MHC class II were also observed. Studies of