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• W2117156688 abstract "The β-galactoside-binding protein galectin-9 is critical in regulating the immune response, but the mechanism by which it functions remains unclear. We have demonstrated that galectin-9 is highly expressed by induced regulatory T cells (iTreg) and was crucial for the generation and function of iTreg cells, but not natural regulatory T (nTreg) cells. Galectin-9 expression within iTreg cells was driven by the transcription factor Smad3, forming a feed-forward loop, which further promoted Foxp3 expression. Galectin-9 increased iTreg cell stability and function by directly binding to its receptor CD44, which formed a complex with transforming growth factor-β (TGF-β) receptor I (TGF-βRI), and activated Smad3. Galectin-9 signaling was further found to regulate iTreg cell induction by dominantly acting through the CNS1 region of the Foxp3 locus. Our data suggest that exogenous galectin-9, in addition to being an effector molecule for Treg cells, acts synergistically with TGF-β to enforce iTreg cell differentiation and maintenance." @default.
• W2117156688 created "2016-06-24" @default.
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• W2117156688 date "2014-08-01" @default.
• W2117156688 modified "2023-10-14" @default.
• W2117156688 title "Galectin-9-CD44 Interaction Enhances Stability and Function of Adaptive Regulatory T Cells" @default.
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• W2117156688 doi "https://doi.org/10.1016/j.immuni.2014.06.011" @default.
• W2117156688 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4219323" @default.
• W2117156688 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25065622" @default.
• W2117156688 hasPublicationYear "2014" @default.
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