We have analyzed the gastrointestinal inflammation which develops following adoptive transfer of IL-4 gene knockout (IL-4 ) CD4 CB45RB (RB ) T cells to severe combined immunodeficient (SCID) or to T cell-deficient, T cell receptor β and δ double knockout (TCR ) mice. Transfer of IL-4 RB T cells induced a similar type of colitis to that seen in SCID or TCR recipients of wild-type (wt) RB T cells as reported previously. Interestingly, transfer of both wt and IL-4 HB T cells to TCR but not to SCID mice induced inflammation in the gastric mucosa. Notably, TCR recipients of IL-4 RB T cells developed a more severe gastritis with erosion, apoptosis of the antral epithelium, and massive infiltration of macrophages. This gastritis was partially dependent on the indigenous microflora. Recipients of both wt and IL-4 RB T cells developed duodenitis with multinuclear giant cells, expansion of mucosal macrophages, and dendritic cells. Full B cell responses were reconstituted in TCR recipients of RB T cells; however, anti-gastric autoantibodies were not detected. We have now developed and characterized a novel model of chronic gastroduodenitis in mice, which will help in our understanding of the mechanisms involved in chronic inflammation in the upper gastrointestinal tract of humans. -/- + Hi Hi -/- -/- Hi -/- Hi -/- Hi -/- -/- -/- Hi -/- Hi -/- Hi
