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从黏膜炎症模型研究中获得的关于口服耐受机制的见解。

Insights into the mechanism of oral tolerance derived from the study of models of mucosal inflammation.

作者信息

Strober Warren, Fuss Ivan, Boirivant Monica, Kitani Atsushi

机构信息

The Mucosal Immunity Section, Laboratory of Host Defense, NIAID, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Ann N Y Acad Sci. 2004 Dec;1029:115-31. doi: 10.1196/annals.1309.029.

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-beta.

摘要

黏膜炎症的小鼠模型通常是由于小鼠无法产生调节性T细胞反应。就这些反应源自口服耐受机制而言,这些模型提供了一种研究口服耐受的独特方式。在本文中,我们重点关注在两种研究最为深入的此类模型(细胞转移模型和三硝基苯磺酸结肠炎模型)中产生的调节性细胞。我们的分析得出这样一种观点,即黏膜炎症中所见的口服耐受所产生的调节性细胞至少部分是识别自身抗原或黏膜微生物群中抗原的细胞,其效应功能依赖于转化生长因子-β的表达。

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