DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, DH | - |
dc.contributor.author | Chang, WS | - |
dc.contributor.author | Lee, YS | - |
dc.contributor.author | Lee, KA | - |
dc.contributor.author | Kim, YK | - |
dc.contributor.author | Kwon, BS | - |
dc.contributor.author | Kang, CY | - |
dc.date.accessioned | 2016-04-01T09:06:28Z | - |
dc.date.available | 2016-04-01T09:06:28Z | - |
dc.date.created | 2009-03-05 | - |
dc.date.issued | 2008-02-15 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.other | 2008-OAK-0000010839 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/29467 | - |
dc.description.abstract | Multiple studies have demonstrated that 4-1BB (CD137), a member of the TNF receptor superfamily, is expressed on several immune cells including activated T cells. However, the expression and the role of 4-1BB on natural killer T (NKT) cells have not been fully characterized. In this study, it was shown that 4-1BB was not expressed on naive NKT cells but was rapidly induced on activated NKT cells by TCR engagement with alpha-galactosylceramide (alpha-GalCer). Also, 4-1BB signaling provided by 3113, an agonistic anti-4-1BB mAb, promoted NKT cell activation resulting in enhanced cytokine production of NKT cells driven by alpha-GalCer. When NKT cell-driven airway immune responses were evaluated by intranasal administration of alpha-GalCer, airway hyperresponsiveness (AHR) and lung inflammation were significantly more aggravated in mice treated with 3113 and alpha-GalCer than in mice treated with alpha-GalCer alone. These aggravations were accompanied by up-regulation of IL-4, IL-13, and IFN-gamma production. Interestingly, AHR was not developed in IL-4R alpha-deficient mice treated with alpha-GalCer with or without 3H3 but was exacerbated in WN-gamma-deficient mice. Our study suggests that 4-1BB on NKT cells functions as a costimulatory molecule and exacerbates the induction of NKT cell-mediated AHR, which is dependent on the IL-4R alpha-mediated pathway. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | AMER ASSOC IMMUNOLOGISTS | - |
dc.relation.isPartOf | JOURNAL OF IMMUNOLOGY | - |
dc.title | 4-1BB engagement costimulates NKT cell activation and exacerbates NKT cell ligand-induced airway hyperresponsiveness and inflammation | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.4049/jimmunol.180.4.2062 | - |
dc.author.google | Kim, DH | - |
dc.author.google | Chang, WS | - |
dc.author.google | Lee, YS | - |
dc.author.google | Lee, KA | - |
dc.author.google | Kim, YK | - |
dc.author.google | Kwon, BS | - |
dc.author.google | Kang, CY | - |
dc.relation.volume | 180 | - |
dc.relation.issue | 4 | - |
dc.relation.startpage | 2062 | - |
dc.relation.lastpage | 2068 | - |
dc.contributor.id | 10103891 | - |
dc.relation.journal | JOURNAL OF IMMUNOLOGY | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCOPUS | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | JOURNAL OF IMMUNOLOGY, v.180, no.4, pp.2062 - 2068 | - |
dc.identifier.wosid | 000253005600015 | - |
dc.date.tcdate | 2019-02-01 | - |
dc.citation.endPage | 2068 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 2062 | - |
dc.citation.title | JOURNAL OF IMMUNOLOGY | - |
dc.citation.volume | 180 | - |
dc.contributor.affiliatedAuthor | Kim, YK | - |
dc.identifier.scopusid | 2-s2.0-42149174964 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 42 | - |
dc.description.isOpenAccess | N | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | KILLER T-CELLS | - |
dc.subject.keywordPlus | ALPHA-GALACTOSYLCERAMIDE | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | CUTTING EDGE | - |
dc.subject.keywordPlus | MONOCLONAL-ANTIBODIES | - |
dc.subject.keywordPlus | ALLERGIC-ASTHMA | - |
dc.subject.keywordPlus | HYPERREACTIVITY | - |
dc.subject.keywordPlus | STIMULATION | - |
dc.subject.keywordPlus | IMMUNITY | - |
dc.subject.keywordPlus | DISEASE | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
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