Aryl hydrocarbon receptor regulates innate and acquired immune resposes

LPS刺激巨噬细胞诱导Ahr。与野生型（WT）细胞相比，ahr缺陷巨噬细胞中LPS产生的IL-6和肿瘤坏死因子(TNF)-α显著升高。在LPS刺激的巨噬细胞中，Ahr与Stat1和核因子κB （NF-κB）形成复合物，从而抑制IL-6启动子活性。因此，Ahr通过与Stat1的相互作用，在LPS信号通路的负调控中起着至关重要的作用。在树突状细胞中，Ahr诱导IDO表达，促进Treg细胞分化。

Ahr is induced in macrophages stimulated by LPS. The production of IL-6 and tumor necrosis factor (TNF)-α by LPS was significantly elevated in Ahr-deficient macrophages compared to that in wild-type (WT) cells. Ahr forms a complex with Stat1 and nuclear factor-kappa B (NF-κB) in macrophages stimulated by LPS, which leads to inhibition of the promoter activity of IL-6. Ahr thus plays an essential role in the negative regulation of the LPS signaling pathway through interaction with Stat1. In dendritic cells, Ahr induces the expression of IDO, which promotes Treg cell differentiation.