Inhibition of peripheral inflammatory disease by carbohydrate antigens derived from normal gut microbiota has been demonstrated for the GI tract, brain, peritoneum, and most recently the airway. We have demonstrated that polysaccharide A (PSA) from the commensal organism Bacteroides fragilis activates CD4⁺ T cells upon presentation by the class II major histocompatibility complex, and that these PSA-experienced T cells prevent the development of lung inflammation in murine models. While the PSA-responding T cells themselves are not canonical FoxP3⁺ regulatory T cells (Tregs), their ability to prevent inflammation is dependent upon the suppressive cytokine IL-10. Using an adoptive T cell transfer approach, we have discovered that PSA-experienced T cells require IL-10 expression by PSA-naïve recipient animals in order to prevent inflammation. A cooperative relationship was found between PSA-activated effector/memory T cells and tissue-resident FoxP3⁺ Tregs both in vivo and in vitro, and it is this cooperation that enables the suppressive activity of PSA outside of the gut environment where exposure takes place. These findings suggest that carbohydrate antigens from the normal microbiota communicate with peripheral tissues to maintain homeostasis through T cell-to-T cell cooperation.

中文翻译：

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多糖经历的效应T细胞诱导FoxP3 ⁺调节性T细胞中的IL-10预防肺部炎症

胃肠道，大脑，腹膜以及最近的气道已证明，源自正常肠道菌群的碳水化合物抗原可抑制周围性炎症。我们已经证明，共生生物脆弱类杆菌（Bacteroides fragilis）的多糖A（PSA）在被II类主要组织相容性复合物呈递后会激活CD4 ⁺ T细胞，并且这些PSA经历过的T细胞可阻止小鼠模型中肺部炎症的发展。响应PSA的T细胞本身不是典型的FoxP3 ⁺调节性T细胞（Tregs），其预防炎症的能力取决于抑制性细胞因子IL-10。使用过继性T细胞转移方法，我们发现PSA经验丰富的T细胞需要未接受过PSA的受者动物表达IL-10，以防止炎症。在体内和体外均发现了PSA激活的效应子/记忆T细胞与驻留在组织中的FoxP3 ⁺ Treg之间的合作关系，正是这种合作使PSA在发生暴露的肠道环境之外具有抑制活性。这些发现表明，来自正常微生物群的碳水化合物抗原与周围组织进行通信，以通过T细胞与T细胞的协作维持体内平衡。