<HashMap><database>GEO</database><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE327115</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Treg-Derived IFN-γ Supports the Differentiation of Th1-Treg in tumor immunity and autoimmunity</name><description>Tregs in tumors are functionally heterogeneous, and Th1-Tregs represent a highly suppressive subset. This study identifies Tregs themselves as a source of IFN-γ, which promotes Th1-Treg differentiation. Treg-derived IFN-γ acts in an autocrine manner to sustain T-bet expression and the Th1-Treg phenotype, while PF4 from Arg1(+) TAMs further amplifies this pathway by inducing Ifng expression in Tregs. Conditional deletion of Ifng in Foxp3(+) cells impaired Th1-Treg differentiation in both tumors and spleen, and a similar mechanism was observed in EAE. Overall, Treg-derived IFN-γ forms a positive feedback loop with other IFN-γ sources and TAM-derived PF4, driving the maintenance and accumulation of Th1-Tregs and reinforcing immunosuppression.</description><dates><publication>2026/06/03</publication></dates><accession>GSE327115</accession><cross_references><GSM>GSM9648570</GSM><GSM>GSM9648571</GSM><GSM>GSM9648572</GSM><GSM>GSM9648573</GSM><GSM>GSM9648574</GSM><GSM>GSM9648575</GSM><GSM>GSM9648576</GSM><GSM>GSM9648577</GSM><GSM>GSM9648568</GSM><GSM>GSM9648569</GSM><GPL>24247</GPL><GSE>327115</GSE><taxon>Mus musculus</taxon><PMID>[42206029]</PMID></cross_references></HashMap>