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- W4386811225 abstract "Targeting PD-1 is an important component of many immune checkpoint blockade (ICB) therapeutic approaches. However, ICB is not an efficacious strategy in a variety of cancer types, in part due to immunosuppressive metabolites in the tumor microenvironment (TME). Here, we find that αPD-1-resistant cancer cells produce abundant itaconate (ITA) due to enhanced levels of aconitate decarboxylase (Acod1). Acod1 has an important role in the resistance to αPD-1, as decreasing Acod1 levels in αPD-1 resistant cancer cells can sensitize tumors to αPD-1 therapy. Mechanistically, cancer cells with high Acod1 inhibit the proliferation of naïve CD8 + T cells through the secretion of inhibitory factors. Surprisingly, inhibition of CD8 + T cell proliferation is not dependent on secretion of ITA, but is instead a consequence of the release of small inhibitory peptides. Our study suggests that strategies to counter the activity of Acod1 in cancer cells may sensitize tumors to ICB therapy." @default.
- W4386811225 created "2023-09-18" @default.
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- W4386811225 date "2023-09-17" @default.
- W4386811225 modified "2023-10-18" @default.
- W4386811225 title "Acod1 Expression in Cancer Cells Promotes Immune Evasion through the Generation of Inhibitory Peptides" @default.
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- W4386811225 doi "https://doi.org/10.1101/2023.09.14.557799" @default.
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