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Cytokine Growth Factor Rev. 2002 Aug-Oct;13(4-5):379-91.

Type I interferons and autoimmunity: lessons from the clinic and from IRF-2-deficient mice.

Author information

1
Department of Molecular Genetics, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chiba 260-8670, Japan. shin-t@sch.md.shinshu-u.ac.jp

Abstract

Type I interferons (IFN-alpha/beta) are produced upon viral and bacterial infections and play essential roles in host defense. However, since IFN-alpha/beta have multiple regulatory functions on innate and adoptive immunity, dysregulation of the IFN-alpha/beta system both in uninfected hosts and during immune responses against infection can result in immunopathologies. In fact, IFN-alpha/beta therapy often accompanies autoimmune-like symptoms. In this regard, we have recently found that mice lacking IFN regulatory factor (IRF)-2, a negative regulator of IFN-alpha/beta signaling, develop spontaneous, CD8(+) T cell-dependent skin inflammation. This unique animal model, together with other animal models, highlights the importance of the mechanism maintaining the homeostasis in the IFN-alpha/beta system even in the absence of infection.

PMID:
12220551
DOI:
10.1016/s1359-6101(02)00023-0
[Indexed for MEDLINE]

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