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

Wei Liang, Jiyu Ding, Qian Chai, Mengjie Lv, Shuting Zheng, Xiangxiang Cao, Zhimin Wang, Xiaoling Ying, Wenqi Wu, Guohong Li and Mingzhao Zhu ()
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Wei Liang: Guangzhou Medical University
Jiyu Ding: Chinese Academy of Sciences
Qian Chai: Chinese Academy of Sciences
Mengjie Lv: Chinese Academy of Sciences
Shuting Zheng: Chinese Academy of Sciences
Xiangxiang Cao: Chinese Academy of Sciences
Zhimin Wang: Chinese Academy of Sciences
Xiaoling Ying: Guangzhou Medical University
Wenqi Wu: Guangzhou Medical University
Guohong Li: Chinese Academy of Sciences
Mingzhao Zhu: Chinese Academy of Sciences

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract 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.

Date: 2025
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DOI: 10.1038/s41467-025-62976-4

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