Loss of YTHDF2 enhances Th9 programming and CAR-Th9 cell antitumor efficacy – New Study
Nature Immunology, Published online: 18 August 2025; doi:10.1038/s41590-025-02235-2
The authors show that the m6A reader protein YTHDF2 negatively regulates Th9 cell differentiation and function. Ablation of YTHDF2 promotes antigen-specific Th9 cell and CAR-Th9 cell antitumor activity in solid tumors.
Summary
A study in Nature Immunology reveals that the m6A reader protein YTHDF2 inhibits the development and function of Th9 cells, a type of immune cell. Specifically, removing YTHDF2 boosts the production of antigen-specific Th9 cells. Furthermore, the absence of YTHDF2 enhances the anti-tumor activity of both regular Th9 cells and engineered CAR-Th9 cells in solid tumor models, suggesting a potential therapeutic target for cancer immunotherapy. This research indicates YTHDF2 blockade could improve Th9-based cancer treatments.
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