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• W1985332778 startingPage "2987" @default.
• W1985332778 abstract "Abstract Effector Th1 cells perpetuate inflammatory damage in a number of autoimmune diseases, including MS and its animal model EAE. Recently, a self‐regulatory mechanism was described in which effector Th1 cells produce the immunomodulatory cytokine IL‐10 to dampen the inflammatory response in both normal and autoimmune inflammation. While the presence of TGF‐β has been suggested to enhance and stabilize an IFN‐γ + IL‐10 + phenotype, the molecular mechanism is poorly understood. Additionally, in the context of adoptive transfer EAE, it is unclear whether IL‐10 acts on the transferred Th1 cells or on endogenous host cells. In the present study, using myelin‐specific TCR‐Tg mice, we show that repetitive Ag stimulation of effector Th1 cells in the presence of TGF‐β increases the population of IFN‐γ + IL‐10 + cells, which correlates with a decrease in EAE severity. Additionally, TGF‐β signaling causes binding of Smad4 to the IL‐10 promoter, providing molecular evidence for TGF‐β‐mediated IL‐10 production from Th1 effector cells. Finally, this study demonstrates that IL‐10 not only reduces encephalitogenic markers such as IFN‐γ and T‐bet on Th1 effector cells expressing the IL‐10R but also prevents recruitment of both transferred and host‐derived inflammatory T cells. These data establish a regulatory mechanism by which highly activated Th1 effector cells modulate their pathogenicity through the induction of IL‐10." @default.
• W1985332778 created "2016-06-24" @default.
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• W1985332778 date "2011-08-30" @default.
• W1985332778 modified "2023-10-18" @default.
• W1985332778 title "TGF-β signaling via Smad4 drives IL-10 production in effector Th1 cells and reduces T-cell trafficking in EAE" @default.
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• W1985332778 doi "https://doi.org/10.1002/eji.201141666" @default.
• W1985332778 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3478765" @default.
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• W1985332778 hasPublicationYear "2011" @default.
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