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 hyper-responsiveness to antigen stimulation, accompanied with a notable upregulation of the expression of genes induced by interferon-alpha/beta (IFN-alpha/beta). Furthermore, both disease development and CD8(+) T cell abnormality are suppressed by the introduction of nullizygosity to the genes that positively regulate the IFN-alpha/beta signaling pathway. IRF-2 may represent a unique negative regulator, attenuating IFN-alpha/beta-induced gene transcription, which is necessary for balancing the beneficial and harmful effects of IFN-alpha/beta signaling in the immune system.
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Authors | S Hida, K Ogasawara, K Sato, M Abe, H Takayanagi, T Yokochi, T Sato, S Hirose, T Shirai, S Taki, T Taniguchi |
Journal | Immunity
(Immunity)
Vol. 13
Issue 5
Pg. 643-55
(Nov 2000)
ISSN: 1074-7613 [Print] United States |
PMID | 11114377
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- DNA-Binding Proteins
- Interferon Regulatory Factor-2
- Irf2 protein, mouse
- Repressor Proteins
- Transcription Factors
- Interferons
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Topics |
- Animals
- CD8-Positive T-Lymphocytes
(immunology)
- Cytotoxicity, Immunologic
- DNA-Binding Proteins
(genetics, immunology)
- Gene Expression Regulation
(immunology)
- Interferon Regulatory Factor-2
- Interferons
(genetics, immunology)
- Mice
- Mice, Knockout
- Repressor Proteins
- Signal Transduction
(genetics, immunology)
- Skin Diseases
(etiology, genetics, immunology)
- Transcription Factors
(genetics, immunology)
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