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EZH2 限制 DNA 甲基化并促进急性病毒感染期间的 T 细胞分化。

EZH2 restricts DNA methylation and promotes T differentiation during acute viral infection.

机构信息

Department of Immunology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Institute of Immunology, Third Military Medical University, Chongqing, China.

出版信息

Front Immunol. 2022 Aug 15;13:942465. doi: 10.3389/fimmu.2022.942465. eCollection 2022.

DOI:10.3389/fimmu.2022.942465
PMID:36045674
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9420843/
Abstract

Follicular helper T (T) cells provide specialized help for B cells to ensure optimal humoral immunity. The histone methyltransferase EZH2, as a chromatin repressor, secures the T differentiation by promoting T lineage associated gene expression during acute viral infection, including and . By using conditional deletion murine system, we observed that EZH2 ablation in CD4 T cells was accompanied by aberrant accumulation of DNA methyltransferases (DNMTs) DNMT1 and DNMT3B in T cells. And the loss of EZH2 promoted aggravation of DNA methylation status at locus. Therefore, our findings suggested that EZH2 plays an important role in maintenance of hypomethylation at locus thus affecting T differentiation during acute viral infection.

摘要

滤泡辅助 T（T）细胞为 B 细胞提供专门的帮助，以确保最佳的体液免疫。组蛋白甲基转移酶 EZH2 作为一种染色质抑制剂，通过在急性病毒感染期间促进 T 谱系相关基因的表达，来确保 T 细胞的分化，包括和。通过使用条件性缺失小鼠系统，我们观察到在 CD4 T 细胞中 EZH2 的缺失伴随着 T 细胞中 DNA 甲基转移酶（DNMTs）DNMT1 和 DNMT3B 的异常积累。并且 EZH2 的缺失促进了 基因座处 DNA 甲基化状态的恶化。因此，我们的研究结果表明，EZH2 在维持急性病毒感染期间 基因座处的低甲基化状态方面起着重要作用，从而影响 T 细胞的分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/36c6b067a646/fimmu-13-942465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/396fc149d000/fimmu-13-942465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/45cd896a54c8/fimmu-13-942465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/03e3a0c41d38/fimmu-13-942465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/6b66584ab145/fimmu-13-942465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/36c6b067a646/fimmu-13-942465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/396fc149d000/fimmu-13-942465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/45cd896a54c8/fimmu-13-942465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/03e3a0c41d38/fimmu-13-942465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/6b66584ab145/fimmu-13-942465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee3d/9420843/36c6b067a646/fimmu-13-942465-g005.jpg

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