Given the task definition and input, reply with output. In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

We have previously demonstrated that interleukin (IL)-10deficient (IL-10 knockout [KO]) but not wild-type (WT) mice develop colitis after infection with Helicobacter hepaticus . Here, we show that infected recombination activating gene (RAG) KO mice develop intestinal inflammation after reconstitution with CD4+ T cells from IL-10 KO animals and that the cotransfer of CD4+ T cells from H. hepaticus infected but not uninfected WT mice prevents this colitis. The disease-protective WT CD4+ cells are contained within the CD45RBlow fraction and unexpectedly were found in both the CD25+ and the CD25 subpopulations of these cells, their frequency being higher in the latter. The mechanism by which CD25+ and CD25 CD45RBlow CD4+ cells block colitis involves IL-10 and not transforming growth factor (TGF)-, as treatment with antiIL-10R but not antiTGF- monoclonal antibody abrogated their protective effect. In vitro, CD45RBlow CD4+ cells from infected WT mice were shown to produce IL-10 and suppress interferon- production by IL-10 KO CD4+ cells in an H. hepaticus antigenspecific manner. Together, our data support the concept that H. hepaticus infection results in the induction in WT mice of regulatory T cells that prevent bacteria-induced colitis. The induction of such cells in response to gut flora may be a mechanism protecting normal individuals against inflammatory bowel disease.
Bacteria-triggered CD4+ T Regulatory Cells Suppress Helicobacter hepaticusinduced Colitis