Siddiqui K R R, Powrie F
Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Mucosal Immunol. 2008 Nov;1 Suppl 1:S34-8. doi: 10.1038/mi.2008.43.
There is evidence that Foxp3(+) regulatory T (T(R)) cells contribute to intestinal homeostasis and that deficiencies in this population can lead to chronic intestinal inflammation. Here, we review recent studies that demonstrate that the gut is a site of peripheral generation of T(R) cells. Functionally specialized gut dendritic cell populations promote T(R) cells through a transforming growth factor-beta and retinoic acid-dependent mechanism. Gut-driven T(R) cells may represent a tissue-specific mechanism to broaden the repertoire of T(R) cells focussed on the gut.
有证据表明，Foxp3(+)调节性T（T(R)）细胞有助于肠道稳态，并且该细胞群体的缺陷可导致慢性肠道炎症。在此，我们综述了近期的研究，这些研究表明肠道是T(R)细胞外周生成的场所。功能特化的肠道树突状细胞群体通过转化生长因子-β和视黄酸依赖性机制促进T(R)细胞的生成。肠道驱动的T(R)细胞可能代表一种组织特异性机制，以扩大聚焦于肠道的T(R)细胞库。
