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TDRD3, a Tudor domain-containing protein, regulates <i>Klf2</i>-dependent T<sub>reg</sub> differentiation and function to modulate immune tolerance.


ABSTRACT: Tudor domain-containing protein 3 (TDRD3) functions as a methylarginine reader that relays posttranslational arginine methylation signals to the transcriptional machinery, thereby regulating cellular functions through modulation of gene expression. Regulatory T cells (Tregs) are pivotal for establishing and maintaining immune tolerance. In this study, we demonstrate that mice with Treg-specific deletion of Tdrd3 exhibit severely impaired iTreg, but not thymic Treg, differentiation. Moreover, iTregs, but not thymic Tregs, derived from these mice fail to suppress colitis in adoptive transfer models, indicating compromised inhibitory capacity. Aged Tdrd3-deficient mice also show spontaneous autoinflammation. Mecha

SUBMITTER: Shi Y 

PROVIDER: S-EPMC12829583 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature