Aryl hydrocarbon receptor regulates innate and acquired immune resposes

AHR在内毒素刺激的巨噬细胞中被诱导。与野生型(WT)细胞相比，AhR基因缺陷的巨噬细胞产生的IL-6和肿瘤坏死因子-α显著增加。在脂多糖刺激的巨噬细胞中，AHR与STAT1和核因子-κB形成复合体，从而抑制IL-6的启动子活性。因此，AHR通过与STAT1相互作用，在内毒素信号通路的负性调控中发挥重要作用。在树突状细胞中，AhR诱导IDO的表达，从而促进Treg细胞的分化。

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.