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FOXP3转录因子是维持调节性T细胞(Treg)免疫抑制功能的必要条件。研究发现FOXP3也可在抗原受体激活的非调节性T细胞表达,使其作为Treg的特异性标志受到质疑。实验证明Treg细胞的FOXP3基因座含有多个去甲基化区域,且似乎更有特异性。FOXP3基因表达和蛋白功能发挥随着组蛋白甲基化和乙酰化水平而改变。DNA甲基化转移酶抑制剂(DNMTi)或组蛋白去乙酰化酶抑制剂(HDACi)可诱导具有免疫抑制功能的Treg产生。本文对FOXP3基因表达调控,蛋白修饰后调节其它基因表达过程中的表观遗传学现象及临床应用前景作一综述。
The FOXP3 transcription factor is essential for maintaining the immunosuppressive function of regulatory T cells (Tregs). FOXP3 was also found to be expressed on antigen receptor-activated, non-regulatory T cells, challenging it as a specific marker of Tregs. Experiments have shown that Treg cells have multiple demethylation sites in the FOXP3 locus and appear to be more specific. FOXP3 gene expression and protein function with histone methylation and acetylation levels change. DNA methyltransferase inhibitors (DNMTi) or histone deacetylase inhibitors (HDACi) induce Treg production with immunosuppressive function. This article reviews the regulation of FOXP3 gene expression, the epigenetic changes in the regulation of other genes after protein modification and the prospect of clinical application.