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More MS news articles for January 2004

Impaired Development of CD4+ CD25+ Regulatory T Cells in the Absence of STAT1: Increased Susceptibility to Autoimmune Disease

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14699080&dopt=Abstract

J Exp Med. 2004 Jan 5; 199(1): 25-34
Nishibori T, Tanabe Y, Su L, David M.
Department of Biology, University of California San Diego, Bonner Hall 3138, 9500 Gilman Drive, La Jolla, CA 92093.

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.