期刊
JOURNAL OF IMMUNOLOGY
卷 199, 期 1, 页码 119-128出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1700366
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资金
- Chinese National Key Basic Research Project Grant [2013CB966803]
- National Scientific Foundation of China [81090412, 81270628, 81430002]
- Shanghai Municipal Committee of Science and Technology [09XD1403000]
Innate immunity activation by viral RNA-primed retinoid acid inducible gene-I (Rig-I) in CD4(+) T cells antagonizes TGFb signaling to suppress the differentiation of regulatory T cells (Tregs). However, how viral RNA-unliganded Rig-I (apo-Rig-I) modulates Treg generation remains unclear. In this article, we show that, in the absence of viral infection, Treg differentiation of Rig-I-/- CD4(+) T cells was compromised, in the presence of increased generation of Th17 cells and overactivation of Stat3, a critical regulator tilting the Treg/Th17 cell balance. Mechanistically, apo-Rig-I physically associates with Stat3, thereby inhibiting Jak1's association with Stat3 while facilitating Shp2' s association to inhibit p-Stat3 levels. Interestingly, inhibition of Stat3 ameliorates the Treg/Th17 imbalance and the colitis observed in Rig-I-/- mice. Collectively, these results uncover an independent functional contribution of the apo-Rig-I/Stat3 interaction in the maintenance of Treg/Th17 cell balance.
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