Dihydroxycholesterols such as 7α,25-dihydroxysterols (7α,25-OHC) and 7α,27-OHC are generated from cholesterol by the enzymes CH25H, CYP7B1 and CYP27A1 in steady state but also in the context of inflammation. The G-protein coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2), also known as GPR183, senses these oxysterols and induces chemotactic migration of immune cells towards higher concentrations of these ligands. We recently showed that these ligands are upregulated in the CNS in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis and that EBI2 enhanced early infiltration of encephalitogenic T cells into the CNS. In this short-review we discuss the role of dihydroxysterol-sensing by immune cells in neuroinflammation.

胆固醇CH25H，CYP7B1和CYP27A1在稳定状态下以及在发炎的情况下，均由胆固醇生成二羟基胆固醇，例如7α，25-二羟基甾醇（7α，25-OHC）和7α，27-OHC。G蛋白偶联受体（GPCR）爱泼斯坦-巴尔病毒诱导的基因2（EBI2），也称为GPR183，可感知这些氧固醇并诱导免疫细胞趋向于这些配体更高浓度的趋化迁移。我们最近显示，在实验性自身免疫性脑脊髓炎（EAE）（一种多发性硬化症的动物模型）中，CNS中的这些配体被上调，并且EBI2增强了脑源性T细胞向CNS的早期浸润。在这篇简短的评论中，我们讨论了免疫细胞对二羟基固醇的感应在神经炎症中的作用。