Cited 6 times in
Interleukin-21 receptor signalling is not critically required for imiquimod-induced psoriasiform dermatitis in mice.
DC Field | Value | Language |
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dc.contributor.author | 김태균 | - |
dc.contributor.author | 이민걸 | - |
dc.contributor.author | 김대석 | - |
dc.date.accessioned | 2018-11-16T16:49:53Z | - |
dc.date.available | 2018-11-16T16:49:53Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 0906-6705 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/165371 | - |
dc.description.abstract | Psoriasis is largely mediated by interleukin (IL)-23/T helper (Th) 17 axis, and IL-21 is a pleiotropic cytokine expressed by Th17 cells. Despite previously reported possible pathogenic roles of IL-21 in human psoriasis, we found that IL-21 receptor (IL-21R) signalling was not crucial for imiquimod-induced psoriatic inflammation, using IL-21R-/- mice. The severity of imiquimod-induced psoriatic manifestation and pro-inflammatory Th17 cytokine levels, IL-17A-producing γδ T cells and CD4+ T cells, and in vitro IL-17A production by γδ T cells after IL-23 stimulation was comparable between wild-type and IL-21R-/- mice. Collectively, IL-21R signalling was not critically involved in IMQ-induced psoriatic inflammation despite an increased IL-21 expression in the IMQ-treated mouse skin. Our data may represent the significant differences between human psoriasis and murine psoriasis model, and further studies using other models will be required to elucidate the role of IL-21 in psoriasis pathogenesis. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Munksgaard | - |
dc.relation.isPartOf | EXPERIMENTAL DERMATOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Interleukin-21 receptor signalling is not critically required for imiquimod-induced psoriasiform dermatitis in mice. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Dermatology (피부과학교실) | - |
dc.contributor.googleauthor | Hee Joo Kim | - |
dc.contributor.googleauthor | Sung Hee Kim | - |
dc.contributor.googleauthor | Tae‐Gyun Kim | - |
dc.contributor.googleauthor | Je Yun Park | - |
dc.contributor.googleauthor | Minseok Lee | - |
dc.contributor.googleauthor | Dae Suk Kim | - |
dc.contributor.googleauthor | Min‐Geol Lee | - |
dc.identifier.doi | 10.1111/exd.13481 | - |
dc.contributor.localId | A05324 | - |
dc.contributor.localId | A02779 | - |
dc.relation.journalcode | J00866 | - |
dc.identifier.eissn | 1600-0625 | - |
dc.identifier.pmid | 29220875 | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/full/10.1111/exd.13481 | - |
dc.subject.keyword | IL-17 | - |
dc.subject.keyword | IL-21 receptor knockout mouse | - |
dc.subject.keyword | IL-22 | - |
dc.subject.keyword | IL-23 | - |
dc.subject.keyword | psoriasis | - |
dc.contributor.alternativeName | Kim, Tae-Gyun | - |
dc.contributor.alternativeName | Lee, Min Geol | - |
dc.contributor.affiliatedAuthor | 김태균 | - |
dc.contributor.affiliatedAuthor | 이민걸 | - |
dc.citation.volume | 27 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 191 | - |
dc.citation.endPage | 195 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL DERMATOLOGY, Vol.27(2) : 191-195, 2018 | - |
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