Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 이지희 | * |
dc.contributor.author | 우소연 | * |
dc.contributor.author | 조경아 | * |
dc.date.accessioned | 2016-08-28T12:08:59Z | - |
dc.date.available | 2016-08-28T12:08:59Z | - |
dc.date.issued | 2012 | * |
dc.identifier.issn | 0953-8178 | * |
dc.identifier.other | OAK-8508 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/222402 | - |
dc.description.abstract | Background: The pathogenesis of inflammatory skin disease involves the release of cytokines from keratinocytes, and one of these, IL-1β, has been previously implicated in inflammatory skin disease. T h17 cells, a subset of T h cells involved in autoimmunity and inflammation, possess IL-1β receptors and secrete cytokines such as IL-17 and IL-22 in response to IL-1β stimulation. A mutation in the inflammasome protein NLRP3 (NACHT, LRR and PYD domains-containing protein 3) causes excess production of IL-1β, resulting in an augmentation of T h17-dominant pathology. Methods: To determine the feedback effect, if any, of IL-17 and/or IL-22 on the secretion of IL-1β from keratinocytes, we stimulated the human keratinocyte cell line HaCaT, as well as caspase-1-deficient mice, with IL-17 or IL-22. Results: We found that treatment with IL-17 and IL-22 causes an increase in IL-1β via the activation of NLRP3 by a process that involves the generation of reactive oxygen species. Moreover, skin inflammation induced by IL-17 and IL-22 was lower in caspase-1 knockout (KO) mice relative to that induced by IL-1β treatment. Additionally, skin inflammation induced by the drug imiquimod was lower in caspase-1 KO mice than in wild-type mice. Conclusion: These results indicate that cytokines from T h17 cells may potentiate IL-1β-mediated skin inflammation and result in phenotypic alterations of keratinocytes via a feedback mechanism. © The Japanese Society for Immunology. 2011. All rights reserved. | * |
dc.language | English | * |
dc.title | IL-17 and IL-22 enhance skin inflammation by stimulating the secretion of il-1β by keratinocytes via the ROS-NLRP3-caspase-1 pathway | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 24 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 147 | * |
dc.relation.lastpage | 158 | * |
dc.relation.journaltitle | International Immunology | * |
dc.identifier.doi | 10.1093/intimm/dxr110 | * |
dc.identifier.wosid | WOS:000300722800003 | * |
dc.identifier.scopusid | 2-s2.0-84857511355 | * |
dc.author.google | Cho K.-A. | * |
dc.author.google | Suh J.W. | * |
dc.author.google | Ho Lee K. | * |
dc.author.google | Kang J.L. | * |
dc.author.google | Woo S.-Y. | * |
dc.contributor.scopusid | 이지희(7404517577) | * |
dc.contributor.scopusid | 우소연(7402853365) | * |
dc.contributor.scopusid | 조경아(21734204400) | * |
dc.date.modifydate | 20240222161025 | * |