The past year has seen continued expansion of the understanding of imm
une 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 cytoki
nes from subsets of T-helper cells, were further characterized. It app
ears that cytokines characteristic of T-helper type 1 cells likely pla
y a role in the pathologic inflammation of IBD. Responses to cytokines
, as well as cytokine production, may also be abnormal in IBD. The pot
ential targets and site of production of antineutrophil cytoplasmic an
tibodies have been characterized. Antiepithelial cell antibodies were
investigated as well. A number of animal models of IBD appeared or wer
e further studied in the past year. Thus, accumulating understanding s
uggests that disruption of certain key regulatory mechanisms may resul
t in pathologic immune responses to luminal bacteria, resulting in chr
onic inflammation.