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- W2115879295 abstract "Abstract CD8+ T cells are fundamental for immune-mediated clearance of viral infections and contribute to immune pathology in autoimmune diseases such as type 1 diabetes. To execute these functions, CD8+ T cells must differentiate into CTLs, a process that is precisely regulated by a variety of cytokines, costimulatory molecules, and transcription factors. IL-21 is an IL-2 family cytokine and a growth factor for multiple lymphocyte effector lineages, including cytotoxic CD8+ T cells. Recent studies demonstrate that loss of IL-21 signaling results in reduced viral clearance in models of lymphocytic choriomeningitis virus infection, and also protection from type 1 diabetes in the NOD model. This is most likely the result of impaired CD8+ CTL function in the absence of IL-21 signaling. Currently, the mechanisms by which IL-21 promotes CTL differentiation in CD8+ T cells remain unclear, particularly the identity of the relevant transcription factor(s). We show that IL-21 promotes CTL function in vitro and killing of pancreatic islets in vivo via the use of transgenic mice expressing IL-21 in pancreatic β cells. We demonstrate that IL-21 induces the expression of the transcription factor T-bet in CD8+ T cells, predominantly via STAT1, and that T-bet is required for the induction of cytolytic molecules, including perforin and granzyme B in response to IL-21. Finally, we show that IL-21–induced CTL function is T-bet dependent, as T-bet deficiency results in defective IL-21–dependent cytotoxicity in CD8+ T cells in vitro and in vivo. Thus, IL-21 drives CD8+ CTL differentiation via the actions of the transcription factor T-bet." @default.
- W2115879295 created "2016-06-24" @default.
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- W2115879295 date "2013-04-15" @default.
- W2115879295 modified "2023-10-03" @default.
- W2115879295 title "IL-21 Promotes CD8+ CTL Activity via the Transcription Factor T-bet" @default.
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- W2115879295 doi "https://doi.org/10.4049/jimmunol.1201730" @default.
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