Insights into the mechanism of oral tolerance derived from the study of models of mucosal inflammation.
Murine models of mucosal inflammation are frequently due to the inability of the mouse to mount a regulatory T cell response. To the extent that such responses arise from oral tolerance mechanisms, these models provide a unique way of studying oral tolerance. In this paper we focus on the regulatory cells generated in two of the most well-studied of such models, the cell-transfer model and the TNBS-colitis model. Our analysis leads to the view that regulatory cells generated by the oral tolerance seen in mucosal inflammation are, at least in part, cells that recognize self-antigens or antigens in the mucosal microflora whose effector function relies on the expression of TGF-beta.
Strober
Warren
W
The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, MD 20892, USA. wstrober@niaid.nih.gov
Fuss
Ivan
I
Boirivant
Monica
M
Kitani
Atsushi
A
D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D007108:Immune Tolerance; D018928:Immunity, Mucosal; D007249:Inflammation / Q000276:immunology*; D051379:Mice; D009061:Mouth Mucosa / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D014302:Trinitrobenzenesulfonic Acid
D016207:Cytokines; D014302:Trinitrobenzenesulfonic Acid