# DUSP2 loss expands virtual memory CD8+ T cells and speeds antiviral response, PNAS study

- Published: 2026-11-11 08:22 UTC
- Section: Life & Health › Biology & biochemistry
- Tags: DUSP2 phosphatase, virtual memory CD8+ T cells, innate-like antiviral immunity, RPA complex, RPA2 phosphorylation, R-loop accumulation, chromatin accessibility, EOMES transcriptional program, RPA1 deletion
- URL: https://realtech.media/news/rt-ba496c8efac03900229690fc_dusp2_loss_expands/

**Researchers found that the phosphatase DUSP2 restrains virtual memory CD8+ T cells through the RPA complex and R-loops; without it, these cells respond to virus rapidly without antigen recognition.**

![DUSP2 loss expands virtual memory CD8+ T cells and speeds antiviral response, PNAS study](https://realtech.media/media/2026/11/4b91624ff5acb345.jpg)
*Borsa, M., Barandun, N., Gräbnitz, F. et al., Wikimedia Commons, CC BY 4.0*

A study in Proceedings of the National Academy of Sciences examines how virtual memory CD8+ T (TVM) cells are regulated. These cells have not encountered antigen but can quickly acquire effector function. Using an autoantibody-based screening strategy, the authors identified the phosphatase dual-specificity phosphatase 2 (DUSP2) as a key regulator of TVM cell responses [1].

DUSP2 deficiency enhanced CD8+ T cell–dependent antiviral immunity and promoted expansion of a highly activated CD44 super-high TVM subset [1]. After viral challenge, these cells responded rapidly without antigen recognition and showed stronger effector and cytokine programs. The authors describe this as innate-like antiviral immunity rather than conventional antigen-specific recall [1].

Mechanistically, DUSP2 interacts with the replication protein A (RPA) complex and regulates RPA2 phosphorylation and chromatin association [1]. Disrupting the DUSP2–RPA axis led to R-loop accumulation and higher chromatin accessibility. This activated Eomesodermin (EOMES)-associated transcriptional programs and promoted TVM cell differentiation [1].

T cell–specific deletion of RPA1 reproduced these effects: TVM cells accumulated spontaneously, and effector-like responses appeared rapidly after viral challenge [1]. The authors conclude that a DUSP2–RPA–R-loop axis restrains TVM cell development and innate-like antiviral immunity [1].

## Sources

1. [Proceedings of the National Academy of Sciences](https://doi.org/10.1073/pnas.2620849123)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-ba496c8efac03900229690fc_dusp2_loss_expands/