Specific microbiota direct the differentiation of IL-17-producing T-helper cells in the mucosa of the small intestine.
Specific microbiota direct the differentiation of IL-17-producing T-helper cells in the mucosa of the small intestine.
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DOI：
10.1016/j.chom.2008.09.009
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发表时间：
2008-10-16
影响因子：
30.3
通讯作者：
Littman DR
中科院分区：
文献类型：
--
作者：
Ivanov II;Frutos Rde L;Manel N;Yoshinaga K;Rifkin DB;Sartor RB;Finlay BB;Littman DR
产生IL-17的辅助性T细胞（Th 17）是炎症的有效效应细胞，但关于它们在稳态下体内分化的要求知之甚少。我们发现，特定的肠道微生物群是小肠固有层（LP）中Th 17细胞分化所必需的。Th 17细胞的分化与肠中噬细胞-黄杆菌-拟杆菌属细菌的存在相关，不依赖于TLR、IL-21或IL-23信号传导，但需要TGF-β的适当活化。Th 17细胞诱导细菌的缺乏伴随着LP中Foxp 3+调节性T细胞的增加。我们的研究结果表明，微生物群的组成调节固有层中的Th 17：Treg平衡，从而可能影响肠道免疫力，耐受性和对炎症性肠病的易感性。
IL-17-producing T-helper cells (Th17) are potent effectors of inflammation, but little is known about the requirements for their differentiation in vivo at steady state. We found that specific commensal microbiota are required for Th17 cell differentiation in the lamina propria (LP) of the small intestine. Differentiation of Th17 cells correlated with presence of Cytophaga-Flavobacter-Bacteroidetes bacteria in the intestine, was independent of TLR, IL-21 or IL-23 signaling, but required appropriate activation of TGF-β. Absence of Th17 cell-inducing bacteria was accompanied by increased Foxp3+ regulatory T cells in the LP. Our results suggest that the composition of the microbiota regulates the Th17:Treg balance in the lamina propria and may thus influence intestinal immunity, tolerance, and susceptibility to inflammatory bowel diseases.
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