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首页> 外文期刊>Cellular immunology >Induction of Foxp3+ regulatory T cells with histone deacetylase inhibitors.
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Induction of Foxp3+ regulatory T cells with histone deacetylase inhibitors.

机译：用组蛋白脱乙酰基酶抑制剂诱导Foxp3 +调节性T细胞。

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Histone deacetylase inhibitors are under investigation in the clinic as a new class of anti-cancer therapeutics. While recent studies have also suggested their potential as inhibitors of a wide spectrum of inflammatory reactions, the anti-inflammatory mechanism of action of these compounds is not fully defined. We show here that the histone deacetylase inhibitors MS-275 and SAHA induce the generation of regulatory T cells (Tregs) from anti-CD3/anti-CD28-stimulated human CD4(+)CD25(-) T cells. These Tregs express the regulatory T cell-associated transcription factor Foxp3 and display suppressive activity against CD4(+)CD25(-) T cell proliferation. Topical treatment with histone deacetylase inhibitors also induces Foxp3 expression in the draining lymph nodes and the skin in the context of a murine contact hypersensitivity model. These findings suggest that Treg generation may serve as a novel mechanism by which histone deacetylase inhibitors regulate the immune response, and provide an additional rationale for the use of histone deacetylase inhibitors in the treatment of inflammation.
机译：组蛋白脱乙酰基酶抑制剂正在临床中作为一种新型的抗癌疗法进行研究。尽管最近的研究也表明它们有潜力作为多种炎症反应的抑制剂，但这些化合物的抗炎作用机理尚未完全确定。我们在这里显示，组蛋白脱乙酰基酶抑制剂MS-275和SAHA诱导抗CD3 /抗CD28刺激的人CD4（+）CD25（-）T细胞产生调节性T细胞（Tregs）。这些Tregs表达与T细胞相关的转录因子Foxp3，并显示出对CD4（+）CD25（-）T细胞增殖的抑制活性。在鼠类接触性超敏反应模型的背景下，用组蛋白脱乙酰基酶抑制剂进行局部治疗还可以诱导引流淋巴结和皮肤中的Foxp3表达。这些发现表明，Treg的产生可以作为组蛋白脱乙酰基酶抑制剂调节免疫应答的新机制，并为在治疗炎症中使用组蛋白脱乙酰基酶抑制剂提供了额外的理由。

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