{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["12(4)"],"submitter":["Shi Y"],"pubmed_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 (T<sub>regs</sub>) are pivotal for establishing and maintaining immune tolerance. In this study, we demonstrate that mice with T<sub>reg</sub>-specific deletion of <i>Tdrd3</i> exhibit severely impaired iT<sub>reg</sub>, but not thymic T<sub>reg</sub>, differentiation. Moreover, iT<sub>regs</sub>, but not thymic T<sub>regs</sub>, derived from these mice fail to suppress colitis in adoptive transfer models, indicating compromised inhibitory capacity. Aged <i>Tdrd3</i>-deficient mice also show spontaneous autoinflammation. Mecha"],"journal":["Science advances"],"pagination":["eaea3960"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12829583"],"repository":["biostudies-literature"],"pubmed_title":["TDRD3, a Tudor domain-containing protein, regulates &lt;i&gt;Klf2&lt;/i&gt;-dependent T&lt;sub&gt;reg&lt;/sub&gt; differentiation and function to modulate immune tolerance."],"pmcid":["PMC12829583"],"pubmed_authors":["Eurmsirilerd E","Shen L","Yang Y","Chang R","Tao X","Yuan YC","Wang G","Shang W","Sun Z","Shi Y","Jia Z"],"additional_accession":[]},"is_claimable":false,"name":"TDRD3, a Tudor domain-containing protein, regulates &lt;i&gt;Klf2&lt;/i&gt;-dependent T&lt;sub&gt;reg&lt;/sub&gt; differentiation and function to modulate immune tolerance.","description":"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 (T<sub>regs</sub>) are pivotal for establishing and maintaining immune tolerance. In this study, we demonstrate that mice with T<sub>reg</sub>-specific deletion of <i>Tdrd3</i> exhibit severely impaired iT<sub>reg</sub>, but not thymic T<sub>reg</sub>, differentiation. Moreover, iT<sub>regs</sub>, but not thymic T<sub>regs</sub>, derived from these mice fail to suppress colitis in adoptive transfer models, indicating compromised inhibitory capacity. Aged <i>Tdrd3</i>-deficient mice also show spontaneous autoinflammation. Mecha","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-06T21:49:41.829Z","creation":"2026-06-05T03:11:30.658Z"},"accession":"S-EPMC12829583","cross_references":{"pubmed":["41576154"],"doi":["10.1126/sciadv.aea3960"]}}