Toward understanding the role of aryl hydrocarbon receptor in the immune system: current progress and future trends.
Toward understanding the role of aryl hydrocarbon receptor in the immune system: current progress and future trends.
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DOI：
10.1155/2014/520763
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发表时间：
2014
影响因子：
--
通讯作者：
Hanieh H
中科院分区：
文献类型：
--
作者：
Hanieh H
免疫系统受到控制免疫细胞发育和功能的不同信号通路的调节。越来越多的证据表明，芳烃受体（Ahr）（一种环境响应转录因子）的连接会导致多重串扰，从而能够调节这些途径及其下游响应基因。大多数免疫细胞会对这种调节做出反应，并且许多炎症反应相关基因的上游含有多个异生素反应元件（XRE）盒。积极的研究工作已经使用不同的动物模型研究了 Ahr 在炎症和自身免疫中的生理作用。最近形成的范例表明，2,3,7,8-四氯二苯并-对二恶英（TCDD）或3,3'-二吲哚甲烷（DIM）激活Ahr可促进CD4+Foxp3+调节性T细胞（Treg）的分化并抑制辅助性T细胞（Th）-17，这表明Ahr是一种治疗自身免疫性炎症的创新策略。这些有希望的发现为未来的人类临床实践奠定了基础。这篇综述探讨了 Ahr 在不同免疫细胞区室中的作用的当前知识，特别关注炎症和自身免疫。
The immune system is regulated by distinct signaling pathways that control the development and function of the immune cells. Accumulating evidence suggest that ligation of aryl hydrocarbon receptor (Ahr), an environmentally responsive transcription factor, results in multiple cross talks that are capable of modulating these pathways and their downstream responsive genes. Most of the immune cells respond to such modulation, and many inflammatory response-related genes contain multiple xenobiotic-responsive elements (XREs) boxes upstream. Active research efforts have investigated the physiological role of Ahr in inflammation and autoimmunity using different animal models. Recently formed paradigm has shown that activation of Ahr by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or 3,3′-diindolylmethane (DIM) prompts the differentiation of CD4+Foxp3+ regulatory T cells (Tregs) and inhibits T helper (Th)-17 suggesting that Ahr is an innovative therapeutic strategy for autoimmune inflammation. These promising findings generate a basis for future clinical practices in humans. This review addresses the current knowledge on the role of Ahr in different immune cell compartments, with a particular focus on inflammation and autoimmunity.
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