Mucosal Immunity and Inflammation II. The yin and yang of T cells in intestinal inflammation: pathogenic and protective roles in a mouse colitis model

Inflammatory bowel disease (IBD) is a multifactorial immune disorder of unc ertain etiology. The advent of several mouse models of mucosal inflammation that resemble IBD has provided insight into the mechanisms governing both normal and pathological mucosal immune function. In a widely used adoptive transfer model, the injection into immunodeficient mice of a subset of CD4( +) T lymphocytes, the CD4(+)CD45RB(high) cells, leads to inflammation of th e intestine. Pathogenesis is due in part to the secretion of proinflammator y cytokines. The induction of colitis can be prevented by cotransfer of ano ther CD4(+) subpopulation, the CD4(+)CD45RB(low) T cells. This population b ehaves analogously to the CD4(+)CD45RB(high) population in terms of the acq uisition of activation markers and homing to the host intestine. However, t heir lymphokine profile when activated is different, and anti-inflammatory cytokines secreted and/or induced by CD4(+)CD45RB(low) T cells prevent coli tis. In this themes article, a description of the adoptive transfer model i s given, the factors that promote and prevent colitis pathogenesis are disc ussed, and some controversial aspects of the model are addressed.