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Article: Targeted disruption of IRF-1 or IRF-2 results in abnormal type I IFN gene induction and aberrant lymphocyte development

TitleTargeted disruption of IRF-1 or IRF-2 results in abnormal type I IFN gene induction and aberrant lymphocyte development
Authors
Issue Date1993
Citation
Cell, 1993, v. 75, n. 1, p. 83-97 How to Cite?
AbstractInterferon regulatory factor 1 (IRF-1), a transcriptional activator, and its antagonistic repressor, IRF-2, were originally identified as regulators of the type I interferon (IFN) system. We have generated mice deficient in either IRF-1 or IRF-2 by gene targeting in embryonic stem cells. IRF-1-deficient fibroblasts lacked the normally observed type I IFN induction by poly(I):poly(C), while they induced type I IFN to similar levels as the wild type following Newcastle disease virus (NDV) infection. In contrast, IRF-2-deficient fibroblasts showed up-regulated type I IFN induction by NDV infection. A profound reduction of TCRαβ+ CD4−CD8+ T cells in IRF-1-deficient mice, with a thymocyte developmental defect, reveals a critical role for IRF-1 in T cell development. IRF-2-deficient mice exhibited bone marrow suppression of hematopoiesis and B lymphopoiesis and mortality following lymphocytic choriomeningitis virus infection. © 1993, Cell Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/292416
ISSN
2023 Impact Factor: 45.5
2023 SCImago Journal Rankings: 24.342
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMatsuyama, Toshifumi-
dc.contributor.authorKimura, Tohru-
dc.contributor.authorKitagawa, Motoo-
dc.contributor.authorPfeffer, Klaus-
dc.contributor.authorKawakami, Takatoshi-
dc.contributor.authorWatanabe, Nobumasa-
dc.contributor.authorKündig, Thomas M.-
dc.contributor.authorAmakawa, Ryuichi-
dc.contributor.authorKishihara, Kenji-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorPotter, Julia-
dc.contributor.authorFurlonger, Caren L.-
dc.contributor.authorNarendran, Arumugavadivel-
dc.contributor.authorSuzuki, Haruhiko-
dc.contributor.authorOhashi, Pamela S.-
dc.contributor.authorPaige, Christopher J.-
dc.contributor.authorTaniguchi, Tadatsugu-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:56:26Z-
dc.date.available2020-11-17T14:56:26Z-
dc.date.issued1993-
dc.identifier.citationCell, 1993, v. 75, n. 1, p. 83-97-
dc.identifier.issn0092-8674-
dc.identifier.urihttp://hdl.handle.net/10722/292416-
dc.description.abstractInterferon regulatory factor 1 (IRF-1), a transcriptional activator, and its antagonistic repressor, IRF-2, were originally identified as regulators of the type I interferon (IFN) system. We have generated mice deficient in either IRF-1 or IRF-2 by gene targeting in embryonic stem cells. IRF-1-deficient fibroblasts lacked the normally observed type I IFN induction by poly(I):poly(C), while they induced type I IFN to similar levels as the wild type following Newcastle disease virus (NDV) infection. In contrast, IRF-2-deficient fibroblasts showed up-regulated type I IFN induction by NDV infection. A profound reduction of TCRαβ+ CD4−CD8+ T cells in IRF-1-deficient mice, with a thymocyte developmental defect, reveals a critical role for IRF-1 in T cell development. IRF-2-deficient mice exhibited bone marrow suppression of hematopoiesis and B lymphopoiesis and mortality following lymphocytic choriomeningitis virus infection. © 1993, Cell Press. All rights reserved.-
dc.languageeng-
dc.relation.ispartofCell-
dc.titleTargeted disruption of IRF-1 or IRF-2 results in abnormal type I IFN gene induction and aberrant lymphocyte development-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0092-8674(05)80086-8-
dc.identifier.pmid8402903-
dc.identifier.scopuseid_2-s2.0-0027361463-
dc.identifier.volume75-
dc.identifier.issue1-
dc.identifier.spage83-
dc.identifier.epage97-
dc.identifier.isiWOS:A1993MB66700010-
dc.identifier.issnl0092-8674-

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