FOXP3型
自身免疫
免疫学
炎症
自身免疫性疾病
调节性T细胞
免疫系统
全身炎症
效应器
T细胞
生物
白细胞介素2受体
医学
抗体
作者
Wei Hu,Zhong-Min Wang,Yongqiang Feng,Michail Schizas,Beatrice Hoyos,Joris van der Veeken,Jacob Verter,Regina Bou-Puerto,Alexander Y. Rudensky
标识
DOI:10.1038/s41590-021-01001-4
摘要
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.
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