The considerable number of murine models of the human inflammatory bowel diseases (IBD) now available (CD4 CD45RBhi T cells! SCID, bm reconstituted human CD3e tg, C3H/HeJBir, TcRa KO, IL-2 KO, IL-10 KO, Gai2 KO, TGFb KO, IL-7 tg) has dramatically altered our thinking about the pathogenesis of these conditions and will allow us to address increasingly sophisticated questions in a defined manner. The gastrointestinal (GI) immune system must respond to pathogens yet be unresponsive (tolerant) to commensal organisms and food proteins. Studies using the murine models of IBD have led to the general consensus that human IBD is the result of disruption of this intestinal immunological homeostasis. More particularly, it appears that the normal balance that the gut maintains between inflammatory and regulatory cytokines is perturbed in IBD and that this may result in inappropriate pathological responses to normal intestinal microflora rather than the usual oral tolerance [1±3]. Descriptions of the murine models of IBD and the role of microbial flora have been extensively and expertly reviewed elsewhere [4±6]. Therefore in this brief review we will concentrate on what these systems have been able to tell us about the role of cytokines in the pathogenesis of IBD and how they may help us to address some still unanswered questions with the ultimate aim of improving therapy.