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Bacteria-triggered CD4+ T regulatory cells suppress Helicobacter hepaticus-induced colitis

Kullberg, M.C., Jankovic, D., Gorelick, P.L., Caspar, P., Letterio, J.J., Cheever, A.W. and Sher, A. (2002) Bacteria-triggered CD4+ T regulatory cells suppress Helicobacter hepaticus-induced colitis. Journal of Experimental Medicine, 196 (4). pp. 505-515. ISSN 0022-1007

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Abstract

We have previously demonstrated that interleukin (IL)-10–deficient (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)-ß, as treatment with anti–IL-10R but not anti–TGF-ß monoclonal antibody abrogated their protective effect. In vitro, CD45RBlow CD4+ cells from infected WT mice were shown to produce IL-10 and suppress interferon-{gamma} production by IL-10 KO CD4+ cells in an H. hepaticus antigen–specific 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.

Item Type: Article
Academic Units: The University of York > Hull York Medical School (York)
Depositing User: York RAE Import
Date Deposited: 22 Apr 2009 10:45
Last Modified: 22 Apr 2009 10:45
Published Version: http://dx.doi.org/10.1084/jem.20020556
Status: Published
Publisher: Rockefeller University Press
Identification Number: 10.1084/jem.20020556
URI: http://eprints.whiterose.ac.uk/id/eprint/6655

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