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- W2763719019 abstract "Foxp3+ Tregs possess potent immunosuppressive activity, which is critical for maintaining immune homeostasis and self-tolerance. Defects in Treg development or function result in inadvertent immune activation and autoimmunity. Despite recent advances in Treg biology, we still do not completely understand the molecular and cellular mechanisms governing the development and suppressive function of these cells. Here, we have demonstrated an essential role of the dedicator of cytokinesis 8 (DOCK8), guanine nucleotide exchange factors required for cytoskeleton rearrangement, cell migration, and immune cell survival in controlling Treg fitness and their function. Treg-specific DOCK8 deletion led to spontaneous multiorgan inflammation in mice due to uncontrolled T cell activation and production of proinflammatory cytokines. In addition, we show that DOCK8-deficient Tregs are defective in competitive fitness and in vivo suppressive function. Furthermore, DOCK8 controls IL-2 signaling, crucial for maintenance and competitive fitness of Tregs, via a STAT5-dependent manner. Our study provides potentially novel insights into the essential function of DOCK8 in Tregs and immune regulation, and it explains the autoimmune manifestations associated with DOCK8 deficiency." @default.
- W2763719019 created "2017-10-20" @default.
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- W2763719019 date "2017-10-05" @default.
- W2763719019 modified "2023-10-18" @default.
- W2763719019 title "DOCK8 regulates fitness and function of regulatory T cells through modulation of IL-2 signaling" @default.
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- W2763719019 doi "https://doi.org/10.1172/jci.insight.94275" @default.
- W2763719019 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5841873" @default.
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- W2763719019 hasPublicationYear "2017" @default.
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