FOXP3型
白细胞介素21
白细胞介素3
白细胞介素2受体
转化生长因子β
白细胞介素12
细胞生物学
细胞毒性T细胞
过继性细胞移植
人口
ZAP70型
转化生长因子
T细胞
生物
化学
免疫学
免疫系统
医学
体外
环境卫生
生物化学
作者
Valérie Dardalhon,Amit Awasthi,Hyoung-Joon Kwon,George Galileos,Wenda Gao,Raymond A. Sobel,Meike Mitsdoerffer,Terry B. Strom,Wassim Elyaman,I‐Cheng Ho,Samia J. Khoury,Mohamed Oukka,Vijay K. Kuchroo
出处
期刊:Nature Immunology
[Springer Nature]
日期:2008-11-09
卷期号:9 (12): 1347-1355
被引量:991
摘要
Transcription factor Foxp3 is critical for generating regulatory T cells (T(reg) cells). Transforming growth factor-beta (TGF-beta) induces Foxp3 and suppressive T(reg) cells from naive T cells, whereas interleukin 6 (IL-6) inhibits the generation of inducible T(reg) cells. Here we show that IL-4 blocked the generation of TGF-beta-induced Foxp3(+) T(reg) cells and instead induced a population of T helper cells that produced IL-9 and IL-10. The IL-9(+)IL-10(+) T cells demonstrated no regulatory properties despite producing abundant IL-10. Adoptive transfer of IL-9(+)IL-10(+) T cells into recombination-activating gene 1-deficient mice induced colitis and peripheral neuritis, the severity of which was aggravated if the IL-9(+)IL-10(+) T cells were transferred with CD45RB(hi) CD4(+) effector T cells. Thus IL-9(+)IL-10(+) T cells lack suppressive function and constitute a distinct population of helper-effector T cells that promote tissue inflammation.
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