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• W3196271963 endingPage "1174" @default.
• W3196271963 startingPage "1163" @default.
• W3196271963 abstract "The immunosuppressive function of regulatory T (Treg) cells is dependent on continuous expression of the transcription factor Foxp3. Foxp3 loss of function or induced ablation of Treg cells results in a fatal autoimmune disease featuring all known types of inflammatory responses with every manifestation stemming from Treg cell paucity, highlighting a vital function of Treg cells in preventing fatal autoimmune inflammation. However, a major question remains whether Treg cells can persist and effectively exert their function in a disease state, where a broad spectrum of inflammatory mediators can either inactivate Treg cells or render innate and adaptive pro-inflammatory effector cells insensitive to suppression. By reinstating Foxp3 protein expression and suppressor function in cells expressing a reversible Foxp3 null allele in severely diseased mice, we found that the resulting single pool of rescued Treg cells normalized immune activation, quelled severe tissue inflammation, reversed fatal autoimmune disease and provided long-term protection against them. Thus, Treg cells are functional in settings of established broad-spectrum systemic inflammation and are capable of affording sustained reset of immune homeostasis." @default.
• W3196271963 created "2021-08-30" @default.
• W3196271963 creator A5018117850 @default.
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• W3196271963 date "2021-08-23" @default.
• W3196271963 modified "2023-09-26" @default.
• W3196271963 title "Regulatory T cells function in established systemic inflammation and reverse fatal autoimmunity" @default.
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• W3196271963 doi "https://doi.org/10.1038/s41590-021-01001-4" @default.
• W3196271963 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34426690" @default.

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