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- W4313369040 abstract "Abstract Human liver CD69+CD8+ T cells are ~95% CD103− and ~5% CD103+. Although CD69+CD103+CD8+ T cells show tissue residency and robustly respond to antigens, CD69+CD103−CD8+ T cells are not yet well understood. Here, we report that human liver CD69+CD103−CD8+ T cells exhibit a phenotype of tissue residency and terminal differentiation with hypoxia-inducible factor (HIF)-2α upregulation. CD103− T cells included both hepatotropic and non-hepatotropic viruses-specific cells whereas CD103+ T cells did only hepatotropic virus-specific cells. Although CD103− cells were weaker effectors on a per cell basis than CD103+ cells following T-cell receptor or interleukin-15 stimulation, they remained the major CD69+CD8+ effector population in the liver, surviving with less cell death. HIF-2α inhibitor or knockdown suppressed the effector functions and survival of CD69+CD103−CD8+ T cells. In addition, HIF-2α expression in liver CD69+CD103−CD8+ T cells was significantly increased in patients with acute hepatitis A or liver cirrhosis (LC). In patients with LC, the activation and increased function of liver CD69+CD103− CD8+ T cells were associated with their HIF-2α expression, which could be controlled by HIF-2α inhibition. In summary, we show that human liver CD69+CD103−CD8+ T cells showed terminally differentiated tissue resident phenotype regulated by HIF-2α." @default.
- W4313369040 created "2023-01-06" @default.
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- W4313369040 date "2020-05-01" @default.
- W4313369040 modified "2023-10-16" @default.
- W4313369040 title "Human liver CD69+CD103−CD8+ memory T cells are regulated by HIF-2α" @default.
- W4313369040 doi "https://doi.org/10.4049/jimmunol.204.supp.157.7" @default.
- W4313369040 hasPublicationYear "2020" @default.
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