Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 199, Issue 1, Pages 25-34Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20020509
Keywords
STAT1; EAE; autoimmune disease; regulatory T cells
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Funding
- NCI NIH HHS [R01 CA080105, CA 80105] Funding Source: Medline
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Type I and 11 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.
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