肠道菌群对Th17/Treg免疫平衡和炎症性肠病影响的研究进展

炎症性肠病(inflammatory bowel disease,IBD)是一种慢性、炎症性、自身免疫性疾病,其发病机制尚未明确,目前认为是由宿主易感性基因、环境、肠道菌群等因素的综合作用引发机体异常免疫炎症应答所致。研究证明,CD4^+T细胞分化成的辅助性T细胞17(Th17)以及调节性T细胞(Treg)之间的失衡将导致IBD的发生。近期研究表明肠道菌群除直接参与IBD的发病外,部分菌群可通过分泌炎症细胞因子,或小分子物质如多糖A(polysaccharide A,PSA)、短链脂肪酸(short-chain fatty acids,SCFAs)等介导或影响Th17/Treg分化平衡,进而加重或缓解肠道免疫炎症反应,影响IBD的发病。本文就肠道菌群如何影响Th17/Treg免疫平衡及IBD的发病过程进行了梳理和总结。

The progress of the roles of gut flora in Th17/Treg axis balance and inflammatory bowel diseases

Inflammatory bowel disease(IBD) is a chronic, inflammatory and autoimmune disorder, which arises as a result of the interactions of environment, flora and genetic factors leading to immunological responses and inflammation in the colon and small intestine. Studies have shown that the imbalance between Th17 and Treg differentiated from CD4^+T cells contributes to IBD. Recent studies have shown that intestinal flora, in addition to being directly involved in the pathogenesis of IBD, may mediate or influence the differentiation of Th17/Treg cells by secreting inflammatory cytokines, or small molecular substances such as polysaccharide A(PSA), short-chain fatty acids(SCFAs), thereby aggravating or alleviating the intestinal immune inflammatory response and affecting the pathogenesis of IBD. In this paper, the possible pathways of intestinal flora influencing Th17/Treg immune balance and pathogenesis of IBD will be summarized.