H2A.Z primes an epigenetic landscape for memory CD8+ T cell recall response
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 deposit...
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| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2025-08-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-025-62976-4 |
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| Summary: | 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. |
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| ISSN: | 2041-1723 |