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Article: Deficiency in the transcription factor interferon regulatory factor (IRF)-2 leads to severely compromised development of natural killer and T helper type 1 cells

TitleDeficiency in the transcription factor interferon regulatory factor (IRF)-2 leads to severely compromised development of natural killer and T helper type 1 cells
Authors
KeywordsInterleukin 15
Interferon regulatory factor
Natural killer cell
Leishmania
Th1
Issue Date2000
Citation
Journal of Experimental Medicine, 2000, v. 192, n. 3, p. 325-336 How to Cite?
AbstractInterferon (IFN) regulatory factor (IRF)-2 was originally described as an antagonist of IRF-1-mediated transcriptional regulation of IFN-inducible genes. IRF-1(-/-) mice exhibit defective T helper type 1 (Th1) cell differentiation. We have used experimental leishmaniasis to show that, like IRF-1(-/-) mice, IRF-2(-/-) mice are susceptible to Leishmania major infection due to a defect in Th1 differentiation. Natural killer (NK) cell development is compromised in both IRF-1(-/-) and IRF-2(-/-) mice, but the underlying mechanism differs. NK (but not NK+ T) cell numbers are decreased in IRF-2(-/-) mice, and the NK cells that are present are immature in phenotype. Therefore, like IRF-1, IRF-2 is required for normal generation of Th1 responses and for NK cell development in vivo. In this particular circumstance the absence of IRF-2 cannot be compensated for by the presence of IRF-1 alone. Mechanistically, IRF-2 may act as a functional agonist rather than antagonist of IRF-1 for some, but not all, IFN-stimulated regulatory element (ISRE)-responsive genes.
Persistent Identifierhttp://hdl.handle.net/10722/291537
ISSN
2023 Impact Factor: 12.6
2023 SCImago Journal Rankings: 6.838
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLohoff, Michael-
dc.contributor.authorDuncan, Gordon S.-
dc.contributor.authorFerrick, David-
dc.contributor.authorMittrücker, Hans Willi-
dc.contributor.authorBischof, Susi-
dc.contributor.authorPrechtl, Stefan-
dc.contributor.authorRöllinghoff, Martin-
dc.contributor.authorSchmitt, Edgar-
dc.contributor.authorPahl, Andreas-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:54:35Z-
dc.date.available2020-11-17T14:54:35Z-
dc.date.issued2000-
dc.identifier.citationJournal of Experimental Medicine, 2000, v. 192, n. 3, p. 325-336-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/291537-
dc.description.abstractInterferon (IFN) regulatory factor (IRF)-2 was originally described as an antagonist of IRF-1-mediated transcriptional regulation of IFN-inducible genes. IRF-1(-/-) mice exhibit defective T helper type 1 (Th1) cell differentiation. We have used experimental leishmaniasis to show that, like IRF-1(-/-) mice, IRF-2(-/-) mice are susceptible to Leishmania major infection due to a defect in Th1 differentiation. Natural killer (NK) cell development is compromised in both IRF-1(-/-) and IRF-2(-/-) mice, but the underlying mechanism differs. NK (but not NK+ T) cell numbers are decreased in IRF-2(-/-) mice, and the NK cells that are present are immature in phenotype. Therefore, like IRF-1, IRF-2 is required for normal generation of Th1 responses and for NK cell development in vivo. In this particular circumstance the absence of IRF-2 cannot be compensated for by the presence of IRF-1 alone. Mechanistically, IRF-2 may act as a functional agonist rather than antagonist of IRF-1 for some, but not all, IFN-stimulated regulatory element (ISRE)-responsive genes.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.subjectInterleukin 15-
dc.subjectInterferon regulatory factor-
dc.subjectNatural killer cell-
dc.subjectLeishmania-
dc.subjectTh1-
dc.titleDeficiency in the transcription factor interferon regulatory factor (IRF)-2 leads to severely compromised development of natural killer and T helper type 1 cells-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1084/jem.192.3.325-
dc.identifier.pmid10934221-
dc.identifier.pmcidPMC2193225-
dc.identifier.scopuseid_2-s2.0-0034617994-
dc.identifier.volume192-
dc.identifier.issue3-
dc.identifier.spage325-
dc.identifier.epage336-
dc.identifier.isiWOS:000088708800003-
dc.identifier.issnl0022-1007-

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