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International Immunology, Vol. 15, No. 7, pp. 855-859, July 2003
© 2003 Japanese Society for Immunology

Protection from autoimmune brain inflammation in mice lacking IFN-regulatory factor-1 is associated with Th2-type cytokines

Thorsten Buch1, Claudia Uthoff-Hachenberg1 and Ari Waisman1

1 Laboratory of Molecular Immunology, Institute for Genetics, University of Cologne, Weyertal 121, 50931 Cologne, Germany

Correspondence to: A. Waisman; E-mail: ari{at}uni-koeln.de
Transmitting editor: L. Steinman

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 Th2-type and decreased production of Th1-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 Th2.

Keywords: autoimmunity, experimental autoimmune encephalomyelitis, IFN-regulatory factor-1, Th1, Th2


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