CD8+ T cell-mediated skin disease in mice lacking IRF-2, the transcriptional attenuator of interferon-α/β signaling

Shigeaki Hida, Kouetsu Ogasawara, Kojiro Sato, Masaaki Abe, Hiroshi Takayanagi, Taeko Yokochi, Takeo Sato, Sachiko Hirose, Toshikazu Shirai, Shinsuke Taki, Tadatsugu Taniguchi

Research output: Contribution to journalArticlepeer-review

200 Citations (Scopus)

Abstract

The balanced action of cytokines is known to be critical for the maintenance of homeostatic immune responses. Here, we report the development of an inflammatory skin disease involving CD8+ T cells, in mice lacking the transcription factor, interferon regulatory factor-2 (IRF-2). CD8+ T cells exhibit in vitro hyperresponsiveness to antigen stimulation, accompanied with a notable upregulation of the expression of genes induced by interferon-α/β (IFN-α/β). Furthermore, both disease development and CD8+ T cell abnormality are suppressed by the introduction of nullizygosity to the genes that positively regulate the IFN-α/β signaling pathway. IRF-2 may represent a unique negative regulator, attenuating IFN-α/β-induced gene transcription, which is necessary for balancing the beneficial and harmful effects of IFN-α/β signaling in the immune system.

Original languageEnglish
Pages (from-to)643-655
Number of pages13
JournalImmunity
Volume13
Issue number5
DOIs
Publication statusPublished - 2000
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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