GEO series
Treg-Derived IFN-γ Supports the Differentiation of Th1-Treg in tumor immunity and autoimmunity
GSE327115
Mus musculus
Expression profiling by high throughput sequencing
10 samples
2026/06/03
GPL24247
Summary
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.
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Paper (PMID 42206029) ↗
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