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IFN-γ可增强巨噬细胞对Toll样受体(Toll-like receptors,TLRs)触发的天然免疫反应,但IFN-γ如何增强巨噬细胞对TLR敏感性的机制研究不多。Ivashkiv等发现IFN-γ可以通过抑制TLR4触发的HES1和HEY1的表达,促进巨噬细胞释放细胞因子。此外,研究还发现,IFN-γ致敏可以使组蛋白发生乙酰化修饰,进而促进染色体重塑,调控基因的表达。总之该研究提出了一种新型机制:IFN-γ通过调控细胞代谢和mRNA翻译促进TLR触发的巨噬细胞活化。
IFN-γ can enhance the natural immune responses triggered by Toll-like receptors (TLRs) in macrophages. However, there are few studies on how IFN-γ enhances the sensitivity of macrophages to TLR. Ivashkiv found that IFN-γ can promote the release of cytokines by macrophages by inhibiting the expression of TLR4-triggered HES1 and HEY1. In addition, the study also found that IFN-γ sensitization histone acetylation can be modified, thereby promoting chromosome remodeling, regulating gene expression. In conclusion, the study proposed a new mechanism: IFN-γ promotes TLR-triggered activation of macrophages by regulating cell metabolism and mRNA translation.