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This study aims to explore how the ascorbate-Tet axis regulates naive T-cell quiescence to maintain immune balance and prevent autoimmunity.

The ascorbate-Tet axis is a checkpoint regulator of naive T-cell quiescence 2257733

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This study aims to explore how the ascorbate-Tet axis regulates naive T-cell quiescence to maintain immune balance and prevent autoimmunity.
In vivo CRISPR screening to investigate nutritional factors and epigenetic mechanisms.
Ablation of Slc23a2 in T cells was conducted to evaluate its effects on ascorbate levels and T-cell differentiation.
Mechanistic analyses assessed the role of ascorbate in activating Tet dioxygenases and its impact on TCR signaling.
Ablation of Slc23a2 decreased intracellular ascorbate, increased DNA hypermethylation, and enhanced naive T cell differentiation into effector and memory T cells.
Low-grade autoimmune inflammation was observed, akin to ascorbate deprivation and Tet dioxygenase deletion.
Tcf1 ablation partly mimicked effects of Slc23a2 deficiency, suggesting a pivotal role in regulating naive T-cell activation.

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Randomized trial investigates the role of ascorbate in T-cell quiescence, highlighting immune regulation.

Hao et al. (2026) studied this question.

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