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- W3187322562 abstract "T-cell dysfunction arising upon repeated antigen exposure prevents effective immunity and immunotherapy. Using various clinically and physiologically relevant systems, we show that a prominent feature of PD-1-expressing exhausted T cells is the development of cellular senescence features both in vivo and ex vivo. This is associated with p16INK4a expression and an impaired cell cycle G1 to S-phase transition in repeatedly stimulated T cells. We show that these T cells accumulate DNA damage and activate the p38MAPK signaling pathway, which preferentially leads to p16INK4a upregulation. However, in highly dysfunctional T cells, p38MAPK inhibition does not restore functionality despite attenuating senescence features. In contrast, p16INK4a targeting can improve T-cell functionality in exhausted CAR T cells. Collectively, this work provides insights into the development of T-cell dysfunction and identifies T-cell senescence as a potential target in immunotherapy." @default.
- W3187322562 created "2021-08-16" @default.
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- W3187322562 date "2021-08-09" @default.
- W3187322562 modified "2023-10-17" @default.
- W3187322562 title "p16INK4a Regulates Cellular Senescence in PD-1-Expressing Human T Cells" @default.
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- W3187322562 doi "https://doi.org/10.3389/fimmu.2021.698565" @default.
- W3187322562 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8381277" @default.
- W3187322562 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34434190" @default.
- W3187322562 hasPublicationYear "2021" @default.
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