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CD8(+) T cell-mediated skin disease in mice lacking IRF-2, the transcriptional attenuator of interferon-alpha/beta signaling
Author(s): Hida S, Ogasawara K, Sato K, Abe M, Takayanagi H, Yokochi T, Sato T, Hirose S, Shirai T, Taki S, Taniguchi T
Source: IMMUNITY    Volume: 13    Issue: 5    Pages: 643-655    Published: NOV 2000  
Times Cited: 94     References: 65     
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-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.
Document Type: Article
Language: English
Reprint Address: Taniguchi, T (reprint author), Univ Tokyo, Fac Med, Dept Immunol, Bunkyo Ku, Hongo 7-3-1, Tokyo 1130033, Japan
Addresses:
1. Univ Tokyo, Fac Med, Dept Immunol, Bunkyo Ku, Tokyo 1130033, Japan
2. Juntendo Univ, Sch Med, Dept Pathol, Bunkyo Ku, Tokyo 1130033, Japan
Publisher: CELL PRESS, 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 USA
Subject Category: Immunology
IDS Number: 378RY
ISSN: 1074-7613
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