| First Author | Nishibori T | Year | 2004 |
| Journal | J Exp Med | Volume | 199 |
| Issue | 1 | Pages | 25-34 |
| PubMed ID | 14699080 | Mgi Jnum | J:87436 |
| Mgi Id | MGI:2687121 | Doi | 10.1084/jem.20020509 |
| Citation | Nishibori T, et al. (2004) Impaired Development of CD4+ CD25+ Regulatory T Cells in the Absence of STAT1: Increased Susceptibility to Autoimmune Disease. J Exp Med 199(1):25-34 |
| abstractText | Type I and II interferons (IFNs) exert opposing effects on the progression of multiple sclerosis, even though both IFNs use the signal transducer and activator of transcription 1 (STAT1) as a signaling mediator. Here we report that STAT1-deficient mice expressing a transgenic T cell receptor against myelin basic protein spontaneously develop experimental autoimmune encephalomyelitis with dramatically increased frequency. The heightened susceptibility to this autoimmune disease appears to be triggered by a reduced number as well as a functional impairment of the CD4+ CD25+ regulatory T cells in STAT1-deficient animals. Adoptive transfer of wild-type regulatory T cells into STAT1-deficient hosts is sufficient to prevent the development of autoimmune disease. These results demonstrate an essential role of STAT1 in the maintenance of immunological self-tolerance. |
