Insights into the Mechanism of Oral Tolerance Derived from the Study of Models of Mucosal Inflammation

Authors

  • WARREN STROBER,

    Corresponding author
    1. The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
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  • IVAN FUSS,

    1. The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
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  • MONICA BOIRIVANT,

    1. The Immune-Mediated Diseases Section, Department of Infectious, Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanita, Rome, Italy
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  • ATSUSHI KITANI

    1. The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
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Address for correspondence: W. Strober, The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, NIH, Bethesda, MD 20892. Voice: 301-496-6810; fax: 301-402-2240. wstrober@niaid.nih.gov

Abstract

Abstract: 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-β.

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