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肠道上皮细胞上的非经典MHC I类分子:黏膜串扰的介质

Non-classical MHC class I molecules on intestinal epithelial cells: mediators of mucosal crosstalk.

作者信息

Shao Ling, Kamalu Okebugwu, Mayer Lloyd

机构信息

The Center for Immunobiology, The Mount Sinai School of Medicine, New York, NY 10029, USA.

出版信息

Immunol Rev. 2005 Aug;206:160-76. doi: 10.1111/j.0105-2896.2005.00295.x.

DOI:10.1111/j.0105-2896.2005.00295.x
PMID:16048548
Abstract

The mucosal immune environment consists of a complex combination of lymphoid cells, non-lymphoid cells, and lumenal bacteria. Signals from lumenal bacteria are constantly transmitted to the underlying tissues across the intestinal epithelial barrier. Intestinal epithelial cells (IECs) can sense these signals, integrate them, and interpret them for lamina propria lymphoid populations. One mechanism by which these signals are communicated is by the expression of non-classical major histocompatibility complex (MHC) class I molecules by IECs. Epithelial cells can express a surprising variety of non-classical MHC class I molecules. In some cases, IECs can act as non-professional antigen-presenting cells utilizing the expression of such non-classical MHC class I molecules to directly present bacterial antigens. In other cases, the expression of non-classical MHC class I molecules may act as a co-stimulatory molecule or adhesion molecule that can modify the mucosal immune response. Finally, the expression of these molecules on IECs can lead to a broad array of responses ranging from tolerance to inflammation. Overall, the IEC, via the expression of non-classical MHC class I molecules, is a central mediator of the constant crosstalk between the intestinal lumen and the mucosal immune system.

摘要

黏膜免疫环境由淋巴细胞、非淋巴细胞和腔内细菌的复杂组合构成。腔内细菌发出的信号持续通过肠上皮屏障传递至下方组织。肠上皮细胞(IECs)能够感知这些信号,将其整合并向固有层淋巴细胞群体进行解读。这些信号传递的一种机制是IECs表达非经典主要组织相容性复合体(MHC)I类分子。上皮细胞能够表达种类惊人的非经典MHC I类分子。在某些情况下,IECs可利用此类非经典MHC I类分子的表达作为非专职抗原呈递细胞直接呈递细菌抗原。在其他情况下,非经典MHC I类分子的表达可能作为共刺激分子或黏附分子发挥作用,从而改变黏膜免疫反应。最后,这些分子在IECs上的表达可引发从耐受到炎症等一系列广泛反应。总体而言,IECs通过表达非经典MHC I类分子,成为肠腔与黏膜免疫系统之间持续相互作用的核心调节因子。

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