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- W4313405893 abstract "Abstract Adoptive cell therapy (ACT), a form of immunotherapy, continues to emerge as a novel therapeutic strategy for treating advanced malignancies. New approaches to improve ACT protocols are needed to enhance in vivo persistence of adoptively transferred tumor antigen-specific T cells and overcome tumor-induced immunosuppression and oxidative stress, which remain significant barriers to the clinical success of ACT. Here, we show that exogenous hydrogen sulfide (H2S), an important gaseous signaling molecule, promoted a central memory phenotype with enhanced antioxidant capacity in tumor antigen-specific T cells. In vitro, T cells treated with exogenous H2S upregulated key antioxidant enzymes and molecules associated with stemness while simultaneously downregulating immune checkpoint molecules. H2S-treated T cells also displayed an enhanced reactivity to tumor antigen, with an increase in production of pro-inflammatory cytokines as well as an increase in overall protein translation. H2S-treated T cells also displayed an enhanced ability to combat oxidative stress, with a reduced accumulation of reactive oxygen species and protection against hydrogen peroxide-induced cell death. In an in vivo murine model of melanoma, tumor-reactive T cells conditioned ex vivo with exogenous H2S demonstrated superior tumor control upon ACT. Even greater tumor control was observed when ACT-treated mice were injected systemically with an H2S donor compound. These data provide evidence that anti-tumor T cells exposed to H2S possess an enhanced metabolic and stem-like phenotype that allows them to persist in the immunosuppressive tumor microenvironment and exert greater tumor control upon adoptive transfer into tumor-bearing hosts. Supported by NIH R01 CA236379" @default.
- W4313405893 created "2023-01-06" @default.
- W4313405893 creator A5041139369 @default.
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- W4313405893 date "2022-05-01" @default.
- W4313405893 modified "2023-09-23" @default.
- W4313405893 title "Hydrogen sulfide signaling in promoting the anti-tumor T cell response" @default.
- W4313405893 doi "https://doi.org/10.4049/jimmunol.208.supp.119.09" @default.
- W4313405893 hasPublicationYear "2022" @default.
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