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DC Field | Value | Language |
---|---|---|
dc.citation.endPage | U158 | - |
dc.citation.number | 7 | - |
dc.citation.startPage | 607 | - |
dc.citation.title | NATURE IMMUNOLOGY | - |
dc.citation.volume | 12 | - |
dc.contributor.author | Park, Sung Ho | - |
dc.contributor.author | Park-Min, Kyung-Hyun | - |
dc.contributor.author | Chen, Janice | - |
dc.contributor.author | Hu, Xiaoyu | - |
dc.contributor.author | Ivashkiv, Lionel B. | - |
dc.date.accessioned | 2023-12-22T06:07:36Z | - |
dc.date.available | 2023-12-22T06:07:36Z | - |
dc.date.created | 2019-03-12 | - |
dc.date.issued | 2011-07 | - |
dc.description.abstract | Endotoxin tolerance, a key mechanism for suppressing excessive inflammatory cytokine production, is induced by prior exposure of macrophages to Toll-like receptor (TLR) ligands. Induction of cross-tolerance to endotoxin by endogenous cytokines has not been investigated. Here we show that prior exposure to tumor necrosis factor (TNF) induced a tolerant state in macrophages, with less cytokine production after challenge with lipopolysaccharide (LPS) and protection from LPS-induced death. TNF-induced cross-tolerization was mediated by suppression of LPS-induced signaling and chromatin remodeling. TNF-induced cross-tolerance was dependent on the kinase GSK3, which suppressed chromatin accessibility and promoted rapid termination of signaling via the transcription factor NF-kappa B by augmenting negative feedback by the signaling inhibitors A20 and I kappa B alpha. Our results demonstrate an unexpected homeostatic function for TNF and a GSK3-mediated mechanism for the prevention of prolonged and excessive inflammation. | - |
dc.identifier.bibliographicCitation | NATURE IMMUNOLOGY, v.12, no.7, pp.607 - U158 | - |
dc.identifier.doi | 10.1038/ni.2043 | - |
dc.identifier.issn | 1529-2908 | - |
dc.identifier.scopusid | 2-s2.0-79959373435 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/26385 | - |
dc.identifier.url | https://www.nature.com/articles/ni.2043 | - |
dc.identifier.wosid | 000291936400008 | - |
dc.language | 영어 | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Tumor necrosis factor induces GSK3 kinase-mediated cross-tolerance to endotoxin in macrophages | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.relation.journalResearchArea | Immunology | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | GLYCOGEN-SYNTHASE KINASE-3-BETA | - |
dc.subject.keywordPlus | GENE-SPECIFIC CONTROL | - |
dc.subject.keywordPlus | RHEUMATOID-ARTHRITIS | - |
dc.subject.keywordPlus | TNF-ALPHA | - |
dc.subject.keywordPlus | INFLAMMATORY RESPONSE | - |
dc.subject.keywordPlus | TEMPORAL CONTROL | - |
dc.subject.keywordPlus | DENDRITIC CELLS | - |
dc.subject.keywordPlus | I INTERFERON | - |
dc.subject.keywordPlus | EXPRESSION | - |
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