DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Hun Sik | ko |
dc.contributor.author | Kim, Dong Chan | ko |
dc.contributor.author | Kim, Hong-Mi | ko |
dc.contributor.author | Kwon, Hyung-Joon | ko |
dc.contributor.author | Kwon, Soon Jae | ko |
dc.contributor.author | Kang, Suk-Jo | ko |
dc.contributor.author | Kim, Sun Chang | ko |
dc.contributor.author | Choi, Go-Eun | ko |
dc.date.accessioned | 2016-04-15T03:05:24Z | - |
dc.date.available | 2016-04-15T03:05:24Z | - |
dc.date.created | 2015-09-14 | - |
dc.date.created | 2015-09-14 | - |
dc.date.issued | 2015-08 | - |
dc.identifier.citation | SCIENTIFIC REPORTS, v.5 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | http://hdl.handle.net/10203/203955 | - |
dc.description.abstract | Interferons (IFNs) potentiate macrophage activation typically via a STAT1-dependent pathway. Recent studies suggest a functioning of STAT1-independent pathway in the regulation of gene expression by IFN-gamma, thus pointing to the diversity in cellular responses to IFNs. Many functions of IFNs rely on cross-regulation of the responses to exogenous inflammatory mediators such as TLR ligands. Here we investigated the contribution of STAT1-independent pathway to macrophage activation and its underlying mechanism in the context of combined stimulation of IFN and TLR. We found that TLR-induced production of inflammatory cytokines (TNF-alpha, IL-12) was not simply nullified but was significantly suppressed by signaling common to IFN-gamma and IFN-beta in STAT1-null macrophages. Such a shift in the suppression of TLR response correlated with a sustained STAT3 activation and attenuation of NF-kappa B signaling. Using a JAK2/STAT(3) pathway inhibitor or STAT3-specific siRNA, blocking STAT3 in that context restored TNF-a production and NF-kappa B signaling, thus indicating a functional cross-regulation among STAT1, STAT3, and NF-kappa B. Our results suggest that STAT1 deficiency reprograms IFN signaling from priming toward suppression of TLR response via feedback regulation of STAT3, which may provide a new insight into the host defense response against microbial pathogens in a situation of STAT1 deficiency. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | PATTERN-RECOGNITION RECEPTORS | - |
dc.subject | TOLL-LIKE RECEPTORS | - |
dc.subject | INTERFERON-GAMMA | - |
dc.subject | KAPPA-B | - |
dc.subject | MACROPHAGE ACTIVATION | - |
dc.subject | CELL-DEATH | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | INNATE IMMUNITY | - |
dc.subject | TARGETED DISRUPTION | - |
dc.subject | IL-10 PRODUCTION | - |
dc.title | STAT1 deficiency redirects IFN signalling toward suppression of TLR response through a feedback activation of STAT3 | - |
dc.type | Article | - |
dc.identifier.wosid | 000359932100001 | - |
dc.identifier.scopusid | 2-s2.0-84940188905 | - |
dc.type.rims | ART | - |
dc.citation.volume | 5 | - |
dc.citation.publicationname | SCIENTIFIC REPORTS | - |
dc.identifier.doi | 10.1038/srep13414 | - |
dc.contributor.localauthor | Kang, Suk-Jo | - |
dc.contributor.localauthor | Kim, Sun Chang | - |
dc.contributor.nonIdAuthor | Kim, Hun Sik | - |
dc.contributor.nonIdAuthor | Kim, Dong Chan | - |
dc.contributor.nonIdAuthor | Kim, Hong-Mi | - |
dc.contributor.nonIdAuthor | Kwon, Hyung-Joon | - |
dc.contributor.nonIdAuthor | Kwon, Soon Jae | - |
dc.contributor.nonIdAuthor | Choi, Go-Eun | - |
dc.description.isOpenAccess | Y | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | PATTERN-RECOGNITION RECEPTORS | - |
dc.subject.keywordPlus | TOLL-LIKE RECEPTORS | - |
dc.subject.keywordPlus | INTERFERON-GAMMA | - |
dc.subject.keywordPlus | KAPPA-B | - |
dc.subject.keywordPlus | MACROPHAGE ACTIVATION | - |
dc.subject.keywordPlus | CELL-DEATH | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | INNATE IMMUNITY | - |
dc.subject.keywordPlus | TARGETED DISRUPTION | - |
dc.subject.keywordPlus | IL-10 PRODUCTION | - |
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