The past year has seen continued expansion of the understanding of immune events in inflammatory bowel disease (IBD). New insights have been gained into how macrophages, T cells, and B cells gain access to the mucosal immune compartment. The role of cytokines, particularly cytokines from subsets of T-helper cells, were further characterized. It appears that cytokines characteristic of T-helper type 1 cells likely play a role in the pathologic inflammation of IBD. Responses to cytokines, as well as cytokine production, may also be abnormal in IBD. The potential targets and site of production of antineutrophil cytoplasmic antibodies have been characterized. Antiepithelial cell antibodies were investigated as well. A number of animal models of IBD appeared or were further studied in the past year. Thus, accumulating understanding suggests that disruption of certain key regulatory mechanisms may result in pathologic immune responses to luminal bacteria, resulting in chronic inflammation.