NK cells inhibit T-bet-deficient, autoreactive Th17 cells.
NK cells inhibit T-bet-deficient, autoreactive Th17 cells.
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DOI:
10.1111/j.1365-3083.2012.02773.x
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发表时间:
2012-12
影响因子:
3.7
通讯作者:
Liu R
中科院分区:
文献类型:
--
作者:
Wu W;Shi S;Ljunggren HG;Cava AL;Van Kaer L;Shi FD;Liu R
The differentiation and maintenance of Th17 cells require a unique cytokine milieu and activation of lineage-specific transcription factors. This process appears to be antagonized by the transcription factor T-bet, which controls the differentiation of Th1 cells. Considering that T-bet-deficient (T-bet−/−) mice are largely devoid of natural killer (NK) cells due to a defect in the terminal maturation of these cells, and because NK cells can influence the differentiation of T helper cells, we investigated whether the absence of NK cells in T-bet-deficient mice contributes to the augmentation of autoreactive Th17 cell responses. We show that the loss of T-bet renders the transcription factors Rorc and STAT3 highly responsive to activation by stimuli provided by NK cells. Furthermore, reconstitution of T-bet−/− mice with wild-type NK cells inhibited the development of autoreactive Th17 cells through NK cell-derived production of IFN-γ. These results identify NK cells as critical regulators in the development of autoreactive Th17 cells and Th17-mediated pathology.
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作者:
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通讯作者:
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DOI:
10.1084/jem.192.5.741
发表时间:
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期刊:
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Gocke, Anne R.;Cravens, Petra D.;Lovett-Racke, Amy E.
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