DC Field | Value | Language |
---|---|---|
dc.contributor.author | Choi, JP | - |
dc.contributor.author | Kim, YS | - |
dc.contributor.author | Tae, YM | - |
dc.contributor.author | Choi, EJ | - |
dc.contributor.author | Hong, BS | - |
dc.contributor.author | Jeon, SG | - |
dc.contributor.author | Gho, YS | - |
dc.contributor.author | Zhu, Z | - |
dc.contributor.author | Kim, YK | - |
dc.date.accessioned | 2016-04-01T02:41:20Z | - |
dc.date.available | 2016-04-01T02:41:20Z | - |
dc.date.created | 2010-11-24 | - |
dc.date.issued | 2010-10 | - |
dc.identifier.issn | 0105-4538 | - |
dc.identifier.other | 2010-OAK-0000021979 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/25590 | - |
dc.description.abstract | P>Background: Innate immune response by a viral pathogen-associated molecular pattern dsRNA modulates the subsequent development of adaptive immune responses. Although virus-associated asthma is characterized by noneosinophilic inflammation, the role of Th17 cell response in the development of virus-associated asthma is still unknown. Objective: To evaluate the role of the Th17 cell response and its underlying polarizing mechanisms in the development of an experimental virus-associated asthma. Methods: An experimental virus-associated asthma was created via airway sensitization with ovalbumin (OVA, 75 mu g) and a low (0.1 mu g) or a high (10 mu g) doses of synthetic dsRNA [polyinosine-polycytidylic acid; poly(I:C)]. Transgenic (IL-17-, IL-6-deficient mice) and pharmacologic [a vascular endothelial growth factor receptor (VEGFR) inhibitor] approaches were used to evaluate the roles of Th17 cell responses. Results: After cosensitization with OVA and low-dose poly(I:C), but not with high-dose poly(I:C), inflammation scores after allergen challenge were lower in IL-17-deficient mice than in wild-type (WT) mice. Moreover, inflammation enhanced by low-dose poly(I:C), but not by high-dose poly(I:C), was impaired in IL-6-deficient mice; this phenotype was accompanied by the down-regulation of IL-17 production from T cells from both lymph nodes and lung tissues. Airway exposure of low-dose poly(I:C) enhanced the production of VEGF and IL-6, and the production of IL-6 was blocked by treatment with a VEGFR inhibitor (SU5416). Moreover, the allergen-specific Th17 cell response and subsequent inflammation in the low-dose poly(I:C) model were impaired by the VEGFR inhibitor treatment during sensitization. Conclusions: Airway exposure of low-level dsRNA induces an allergen-specific Th17 cell response, which is mainly dependent on VEGF and IL-6. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | WILEY-BLACKWELL PUBLISHING, INC | - |
dc.relation.isPartOf | ALLERGY | - |
dc.subject | IL-6 | - |
dc.subject | noneosinophilic asthma | - |
dc.subject | Th17 | - |
dc.subject | vascular endothelial growth factor | - |
dc.subject | virus-associated asthma | - |
dc.subject | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject | TOLL-LIKE RECEPTOR-3 | - |
dc.subject | T-HELPER-CELLS | - |
dc.subject | CHILDHOOD ASTHMA | - |
dc.subject | T(H)17 CELLS | - |
dc.subject | RIG-I | - |
dc.subject | INFLAMMATION | - |
dc.subject | INTERLEUKIN-17 | - |
dc.subject | ACTIVATION | - |
dc.subject | DISTINCT | - |
dc.title | A viral PAMP double-stranded RNA induces allergen-specific Th17 cell response in the airways which is dependent on VEGF and IL-6 | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.1111/J.1398-9995.2010.02369.X | - |
dc.author.google | Choi, JP | - |
dc.author.google | Kim, YS | - |
dc.author.google | Tae, YM | - |
dc.author.google | Choi, EJ | - |
dc.author.google | Hong, BS | - |
dc.author.google | Jeon, SG | - |
dc.author.google | Gho, YS | - |
dc.author.google | Zhu, Z | - |
dc.author.google | Kim, YK | - |
dc.relation.volume | 65 | - |
dc.relation.issue | 10 | - |
dc.relation.startpage | 1322 | - |
dc.relation.lastpage | 1330 | - |
dc.contributor.id | 10103891 | - |
dc.relation.journal | ALLERGY | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCI | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | ALLERGY, v.65, no.10, pp.1322 - 1330 | - |
dc.identifier.wosid | 000281631500015 | - |
dc.date.tcdate | 2019-02-01 | - |
dc.citation.endPage | 1330 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 1322 | - |
dc.citation.title | ALLERGY | - |
dc.citation.volume | 65 | - |
dc.contributor.affiliatedAuthor | Gho, YS | - |
dc.identifier.scopusid | 2-s2.0-77956443815 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 19 | - |
dc.description.scptc | 21 | * |
dc.date.scptcdate | 2018-05-121 | * |
dc.type.docType | Article | - |
dc.subject.keywordPlus | ENDOTHELIAL GROWTH-FACTOR | - |
dc.subject.keywordPlus | T-HELPER-CELLS | - |
dc.subject.keywordPlus | T(H)17 CELLS | - |
dc.subject.keywordPlus | RIG-I | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | ASTHMA | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | DISTINCT | - |
dc.subject.keywordPlus | INNATE | - |
dc.subject.keywordPlus | SENSITIZATION | - |
dc.subject.keywordAuthor | IL-6 | - |
dc.subject.keywordAuthor | noneosinophilic asthma | - |
dc.subject.keywordAuthor | Th17 | - |
dc.subject.keywordAuthor | vascular endothelial growth factor | - |
dc.subject.keywordAuthor | virus-associated asthma | - |
dc.relation.journalWebOfScienceCategory | Allergy | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Allergy | - |
dc.relation.journalResearchArea | Immunology | - |
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