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Reply to ‘Comment on: Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation’

Cellular & Molecular Immunology volume 22, pages 559–562 (2025)Cite this article

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Our previous study demonstrated that GSK3 plays an indispensable role in the expansion of effector CD8+ T cells and the regulation of T-cell exhaustion. GSK3 controls T-cell exhaustion by regulating TCR-mediated NFAT activation through promoting the nuclear export of NFAT, thereby restraining NFAT-induced expression of exhaustion-associated genes, including TOX/TOX2 and PD-1 [1].

We thank Dr. Rudd et al. for their careful consideration of our study. They raised very important and critical concerns, and we address these concerns individually below.

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Authors and Affiliations

  1. State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot, Inner Mongolia, China

    Yubing Fu

  2. State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Faculty of Medicine and Life Science, Xiamen University, Xiamen, Fujian, China

    Wen-Hsien Liu

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  1. Yubing Fu
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  2. Wen-Hsien Liu
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Correspondence to Yubing Fu or Wen-Hsien Liu.

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Fu, Y., Liu, WH. Reply to ‘Comment on: Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation’. Cell Mol Immunol 22, 559–562 (2025). https://doi.org/10.1038/s41423-025-01280-z

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