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The Chromatin-Modifying Enzyme Ezh2 Is Critical for the Maintenance of Regulatory T Cell Identity after Activation

机译：染色质修饰酶Ezh2对于激活后维持调节性T细胞身份至关重要

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Regulatory T cells (Treg cells) are required for immune homeostasis. Chromatin remodeling is essential for establishing diverse cellular identities, but how the epigenetic program in Treg cells is maintained throughout the dynamic activation process remains unclear. Here we have shown that CD28 co-stimulation, an extracellular cue intrinsically required for Treg cell maintenance, induced the chromatin-modifying enzyme, Ezh2. Treg-specific ablation of Ezh2 resulted in spontaneous autoimmunity with reduced Foxp3(+) cells in non-lymphoid tissues and impaired resolution of experimental autoimmune encephalomyelitis. Utilizing a model designed to selectively deplete wild-type Treg cells in adult mice co-populated with Ezh2-deficient Treg cells, Ezh2-deficient cells were destabilized and failed to prevent autoimmunity. After activation, the transcriptome of Ezh2-deficient Treg cells was disrupted, with altered expression of Treg cell lineage genes in a pattern similar to Foxp3-deficient Treg cells. These studies reveal a critical role for Ezh2 in the maintenance of Treg cell identity during cellular activation.
机译：免疫稳态需要调节性T细胞（Treg细胞）。染色质重塑对于建立各种细胞身份至关重要，但是如何在动态激活过程中维持Treg细胞的表观遗传程序仍然不清楚。在这里，我们显示了CD28共刺激（Treg细胞维持所固有的胞外信号）诱导了染色质修饰酶Ezh2。 Ezh2的Treg特异性消融导致非淋巴组织中Foxp3（+）细胞减少的自发性自身免疫和实验性自身免疫性脑脊髓炎的分辨率降低。利用设计为选择性消耗与Ezh2缺陷型Treg细胞共存的成年小鼠的野生型Treg细胞的模型，Ezh2缺陷型细胞不稳定，无法预防自身免疫。激活后，Ezh2缺陷型Treg细胞的转录组被破坏，Treg细胞谱系基因表达的改变与Foxp3缺陷型Treg细胞类似。这些研究揭示了Ezh2在细胞激活过程中维持Treg细胞身份的关键作用。

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