Dysregulated cytokine production by mucosal lymphocytes and macrophages has been implicated in the pathogenesis of both Crohn’s disease and ulcerative colitis, the two major forms of human inflammatory bowel disease (IBD).1 Over the past few years, various murine models of chronic intestinal inflammation resembling IBD have been discovered which have provided important clues as to the nature of this dysregulation and to its possible treatment with cytokines.2 Thus, in studies of several of the models most closely resembling Crohn’s disease it has been shown that production of large amounts of Th1-type cytokines—for example, interferon γ, by T cells is a major and essential feature of the inflammation.2 In addition, it has been shown that this disease causing Th1 cytokine response can be counteracted by induction of a suppressor response involving the generation of T cells producing Th2-type cytokines or transforming growth factor …