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- W4313405728 startingPage "119.11" @default.
- W4313405728 abstract "Abstract Tumors infiltrated with abundant T lymphocytes are generally thought to respond to immune checkpoint inhibitors (ICI). However, a significant proportion of immune hot tumors are resistant to ICI. The immune nature of such tumors is poorly understood. We recently reported a tumor type that is defective in transcription elongation (TEdef) and irresponsive to ICI in several clinical cohorts. Here, we show that TEdef tumors are unexpectedly infiltrated with cytotoxic T cells (CTLs) in patients and in animal models. Mechanistically, T cell infiltration is facilitated by cytoplasmic DNA/double strand RNA-nucleic acid sensing-TBK1-ccl5/cxcl/9/10 signaling cascade. However, single-cell RNA sequencing combined with flow cytometry reveals that CTLs in TEdef tumors are exhausted. Furthermore, immune suppressive regulatory T cells are enriched in TEdef tumors. ICI treatment of TEdef tumors in mice and human patients fails to further induce T cell infiltration. This study reveals a mechanism underlying inert inflammation and ICI resistance of TEdef tumors. We suggest that TEdef, alongside the surrogate markers of tumor mutational burden and CTLs, should be assessed in immunotherapy-candidate patients. Supported by 5R01CA234038-03" @default.
- W4313405728 created "2023-01-06" @default.
- W4313405728 creator A5001430135 @default.
- W4313405728 creator A5005625979 @default.
- W4313405728 date "2022-05-01" @default.
- W4313405728 modified "2023-09-29" @default.
- W4313405728 title "Tumors bearing defective transcription elongation are immune hot but resistant to immune checkpoint inhibitors" @default.
- W4313405728 doi "https://doi.org/10.4049/jimmunol.208.supp.119.11" @default.
- W4313405728 hasPublicationYear "2022" @default.
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