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- Publisher Website: 10.1084/jem.192.3.325
- Scopus: eid_2-s2.0-0034617994
- PMID: 10934221
- WOS: WOS:000088708800003
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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
Title | Deficiency in the transcription factor interferon regulatory factor (IRF)-2 leads to severely compromised development of natural killer and T helper type 1 cells |
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Authors | |
Keywords | Interleukin 15 Interferon regulatory factor Natural killer cell Leishmania Th1 |
Issue Date | 2000 |
Citation | Journal of Experimental Medicine, 2000, v. 192, n. 3, p. 325-336 How to Cite? |
Abstract | Interferon (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 Identifier | http://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 Field | Value | Language |
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dc.contributor.author | Lohoff, Michael | - |
dc.contributor.author | Duncan, Gordon S. | - |
dc.contributor.author | Ferrick, David | - |
dc.contributor.author | Mittrücker, Hans Willi | - |
dc.contributor.author | Bischof, Susi | - |
dc.contributor.author | Prechtl, Stefan | - |
dc.contributor.author | Röllinghoff, Martin | - |
dc.contributor.author | Schmitt, Edgar | - |
dc.contributor.author | Pahl, Andreas | - |
dc.contributor.author | Mak, Tak W. | - |
dc.date.accessioned | 2020-11-17T14:54:35Z | - |
dc.date.available | 2020-11-17T14:54:35Z | - |
dc.date.issued | 2000 | - |
dc.identifier.citation | Journal of Experimental Medicine, 2000, v. 192, n. 3, p. 325-336 | - |
dc.identifier.issn | 0022-1007 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291537 | - |
dc.description.abstract | Interferon (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.language | eng | - |
dc.relation.ispartof | Journal of Experimental Medicine | - |
dc.subject | Interleukin 15 | - |
dc.subject | Interferon regulatory factor | - |
dc.subject | Natural killer cell | - |
dc.subject | Leishmania | - |
dc.subject | Th1 | - |
dc.title | Deficiency in the transcription factor interferon regulatory factor (IRF)-2 leads to severely compromised development of natural killer and T helper type 1 cells | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1084/jem.192.3.325 | - |
dc.identifier.pmid | 10934221 | - |
dc.identifier.pmcid | PMC2193225 | - |
dc.identifier.scopus | eid_2-s2.0-0034617994 | - |
dc.identifier.volume | 192 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 325 | - |
dc.identifier.epage | 336 | - |
dc.identifier.isi | WOS:000088708800003 | - |
dc.identifier.issnl | 0022-1007 | - |