T cell-intrinsic and -extrinsic contributions of the IFNAR/STAT1-axis to thymocyte survival.

T cell-intrinsic and -extrinsic contributions of the IFNAR/STAT1-axis to thymocyte survival.
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DOI:
10.1371/journal.pone.0024972
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发表时间:
2011
期刊:
影响因子:
3.7
通讯作者:
David M
David M
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Moro H;Otero DC;Tanabe Y;David M

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STAT1 is an essential part of interferon signaling, and STAT1-deficiency results in heightened susceptibility to infections or autoimmunity in both mice and humans. Here we report that mice lacking the IFNα/β-receptor (IFNAR1) or STAT1 display impaired deletion of autoreactive CD4+CD8+-T-cells. Strikingly, co-existence of WT T cells restored thymic elimination of self-reactive STAT1-deficient CD4+CD8+-T cells. Analysis of STAT1-deficient thymocytes further revealed reduced Bim expression, which was restored in the presence of WT T cells. These results indicate that type I interferons and STAT1 play an important role in the survival of MHC class I-restricted T cells in a T cell intrinsic and non-cell intrinsic manner that involves regulation of Bim expression through feedback provided by mature STAT1-competent T cells.
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