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<p>The rapid recall ability is a hallmark of memory CD8<sup>+</sup> T cells, but the underlying mechanisms remain incompletely understood. Here we find that histone variant H2A.Z is expressed at higher levels in memory CD8<sup>+</sup> T cells than in naïve cells. Furthermore, in memory CD8<sup>+</sup> T cells H2A.Z is deposited at the promoters and enhancers, particularly super enhancers, of those genes involved in recall responses, while H2A.Z deficiency in memory CD8<sup>+</sup> T cells inhibits recall responses in vitro and in vivo. Mechanistically, multi-omics analyses show that H2A.Z maintains a poised epigenetic landscape on those recall response genes to potentiate a rapid transcription activation. Accordingly, H2A.Z deposition on these genes is induced by TCR/CD28 signals, and is cooperated by IL-7/IL-15 signals. Together, our data suggest that H2A.Z may orchestrate a specific epigenetic landscape during memory T cell differentiation to facilitate a rapid recall response.</p>

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H2A.Z primes an epigenetic landscape for memory CD8+ T cell recall response

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月15日

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  • Wei Liang,
  • Jiyu Ding,
  • Qian Chai,
  • Mengjie Lv,
  • Shuting Zheng,
  • Xiangxiang Cao,
  • Zhimin Wang,
  • Xiaoling Ying,
  • Wenqi Wu,
  • Guohong Li,
  • Mingzhao Zhu

摘要

The rapid recall ability is a hallmark of memory CD8+ T cells, but the underlying mechanisms remain incompletely understood. Here we find that histone variant H2A.Z is expressed at higher levels in memory CD8+ T cells than in naïve cells. Furthermore, in memory CD8+ T cells H2A.Z is deposited at the promoters and enhancers, particularly super enhancers, of those genes involved in recall responses, while H2A.Z deficiency in memory CD8+ T cells inhibits recall responses in vitro and in vivo. Mechanistically, multi-omics analyses show that H2A.Z maintains a poised epigenetic landscape on those recall response genes to potentiate a rapid transcription activation. Accordingly, H2A.Z deposition on these genes is induced by TCR/CD28 signals, and is cooperated by IL-7/IL-15 signals. Together, our data suggest that H2A.Z may orchestrate a specific epigenetic landscape during memory T cell differentiation to facilitate a rapid recall response.