Inflammatory bowel disease (IBD) is thought to result from a dysregulated mucosal immune response to luminal microbial antigens, with T lymphocytes mediating the colonic pathology. Infection with Helicobacter spp has been reported to cause IBD in immunodeficient mice, some of which lack T lymphocytes. To further understand the role of T cells and microbial antigens in triggering IBD, we infected interleukin (IL)-10^−/−, recombinase-activating gene (Rag)1^−/−, T-cell receptor (TCR)-α^−/−, TCR-β^−/−, and wild-type mice with Helicobacter hepaticus orHelicobacter bilis and compared the histopathological IBD phenotype. IL-10^−/− mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1^−/−, TCR-α^−/−, TCR-β^−/−, and wild-type mice showed different susceptibilities to Helicobacter spp infection. Proinflammatory cytokine mRNA expression was increased in the colons ofHelicobacter-infected IL-10^−/− and TCR-α^−/− mice with IBD. These results confirm and extend the role of Helicobacter as a useful tool for investigating microbial-induced IBD and show the importance, but not strict dependence, of T cells in the development of bacterial-induced IBD.