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More MS news articles for June 2003

Protection from autoimmune brain inflammation in mice lacking IFN-regulatory factor-1 is associated with T(h)2-type cytokines

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12807824&dopt=Abstract

Int Immunol. 2003 Jul;15(7):855-9
Buch T, Uthoff-Hachenberg C, Waisman A.
Laboratory of Molecular Immunology, Institute for Genetics, University of Cologne, Weyertal 121, 50931 Cologne, Germany.

IFN-regulatory factor-1 (IRF-1) is a transcription factor that regulates the expression of IFN-induced genes and type I IFN.

It has previously been demonstrated that IRF-1-deficient mice show reduced susceptibility to experimental autoimmune encephalomyelitis (EAE) induced by a peptide from myelin basic protein.

To further study the role of IRF-1 in brain inflammation, we analyzed EAE induced by immunization with a myelin oligodendrocyte glycoprotein-derived peptide in 129/Sv mice lacking IRF-1.

We found that these mice were almost completely resistant to EAE induction and that this unresponsiveness was intrinsically related to the IRF-1 deficiency of the T cells, but not with any other cell type.

Furthermore, we show that the amelioration of EAE was associated with increased production of T(h)2-type and decreased production of T(h)1-type cytokines.

These results demonstrate that absence of IRF-1 in myelin-specific T cells results in protection from severe EAE and is associated with a skewing of the T cell response towards T(h)2.