Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17-producing T cell responses
Lamina propria macrophages and dendritic cells differentially induce regulatory and interleukin 17-producing T cell responses
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DOI：
10.1038/ni1511
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发表时间：
2007-10-01
影响因子：
30.5
通讯作者：
Pulendran, Bali
中科院分区：
文献类型：
--
作者：
Denning, Timothy L.;Wang, Yi-Chong;Pulendran, Bali
肠道免疫系统必须引发针对有害病原体的强大免疫力，但也必须抑制针对肠道微生物和饮食抗原的免疫应答。维持这种二分法的机制知之甚少。在这里，我们描述了一个群体的CD 11b（+）F4/80（+）CD 11 c（-）巨噬细胞在固有层表达几种抗炎分子，包括白细胞介素10（IL-10），但很少或没有促炎细胞因子，即使在刺激后与Toll样受体配体。这些巨噬细胞通过依赖于IL-10、视黄酸和外源性转化生长因子β的机制诱导Foxp 3（+）调节性T细胞的分化。相反，固有层CD 11b（+）树突状细胞引起IL-17的产生。这种IL-17的产生被固有层巨噬细胞抑制，表明这些亚群之间的动态相互作用可能影响免疫激活和耐受之间的平衡。
The intestinal immune system must elicit robust immunity against harmful pathogens but must also restrain immune responses directed against commensal microbes and dietary antigens. The mechanisms that maintain this dichotomy are poorly understood. Here we describe a population of CD11b(+)F4/80(+)CD11c(-) macrophages in the lamina propria that expressed several anti-inflammatory molecules, including interleukin 10 (IL-10), but little or no proinflammatory cytokines, even after stimulation with Toll-like receptor ligands. These macrophages induced, by a mechanism dependent on IL-10, retinoic acid and exogenous transforming growth factor-beta, the differentiation of Foxp3(+) regulatory T cells. In contrast, lamina propria CD11b(+) dendritic cells elicited IL-17 production. This IL-17 production was suppressed by lamina propria macrophages, indicating that a dynamic interaction between these subsets may influence the balance between immune activation and tolerance.