| First Author | Moro H | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 9 | Pages | e24972 |
| PubMed ID | 21949815 | Mgi Jnum | J:177873 |
| Mgi Id | MGI:5296424 | Doi | 10.1371/journal.pone.0024972 |
| Citation | Moro H, et al. (2011) T cell-intrinsic and -extrinsic contributions of the IFNAR/STAT1-axis to thymocyte survival. PLoS One 6(9):e24972 |
| abstractText | 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 IFNalpha/beta-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. |
