DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, SW | - |
dc.contributor.author | Park, Y | - |
dc.contributor.author | Eun, SY | - |
dc.contributor.author | Madireddi, S | - |
dc.contributor.author | Cheroutre, H | - |
dc.contributor.author | Croft, M | - |
dc.date.accessioned | 2016-03-31T08:45:32Z | - |
dc.date.available | 2016-03-31T08:45:32Z | - |
dc.date.created | 2013-03-05 | - |
dc.date.issued | 2012-09-15 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.other | 2012-OAK-0000026664 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/15984 | - |
dc.description.abstract | Dendritic cells (DC) in the gut promote immune tolerance by expressing retinal dehydrogenase (RALDH), an enzyme that promotes retinoic acid, which aids differentiation of Foxp3(+) inducible regulatory T cells (iTreg) in the intestinal mucosa. How RALDH expression is regulated is unclear. We found that 4-1BB (CD137), a member of the TNFR family, together with CD103, marked mesenteric lymph node DC with the highest level of RALDH activity, and ligation of 4-1BB maintained RALDH expression in these gut DC. Moreover, 4-1BB signals synergized with those through TLR2 or GM-CSFR to promote RALDH activity in undifferentiated DC. Correspondingly, 4-1BB-deficient mice were impaired in their ability to generate iTreg in the GALT when exposed to oral Ag, and 4-1BB-deficient mesenteric lymph node DC displayed weak RALDH activity and were poor at promoting iTreg development. Thus, our data demonstrate a novel activity of 4-1BB in controlling RALDH expression and the regulatory activity of DC. The Journal of Immunology, 2012, 189: 2697-2701. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | The American Association of Immunologists. | - |
dc.relation.isPartOf | JOURNAL OF IMMUNOLOGY | - |
dc.subject | T-CELLS | - |
dc.subject | IMMUNE REGULATION | - |
dc.subject | VITAMIN-A | - |
dc.subject | ACID | - |
dc.subject | DIFFERENTIATION | - |
dc.subject | RESPONSES | - |
dc.subject | MICROBIOTA | - |
dc.subject | INDUCTION | - |
dc.subject | SYSTEM | - |
dc.title | 4-1BB Cutting Edge: Controls Regulatory Activity in Dendritic Cells through Promoting Optimal Expression of Retinal Dehydrogenase. | - |
dc.type | Article | - |
dc.contributor.college | 융합생명공학부 | - |
dc.identifier.doi | 10.4049/jimmunol.1201248 | - |
dc.author.google | Lee, SW | - |
dc.author.google | Park, Y | - |
dc.author.google | Eun, SY | - |
dc.author.google | Madireddi, S | - |
dc.author.google | Cheroutre, H | - |
dc.author.google | Croft, M | - |
dc.relation.volume | 189 | - |
dc.relation.startpage | 2687 | - |
dc.relation.lastpage | 2701 | - |
dc.contributor.id | 10113012 | - |
dc.relation.journal | JOURNAL OF IMMUNOLOGY | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCI | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | JOURNAL OF IMMUNOLOGY, v.189, no.6, pp.2687 - 2701 | - |
dc.identifier.wosid | 000308698600002 | - |
dc.date.tcdate | 2019-01-01 | - |
dc.citation.endPage | 2701 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 2687 | - |
dc.citation.title | JOURNAL OF IMMUNOLOGY | - |
dc.citation.volume | 189 | - |
dc.contributor.affiliatedAuthor | Lee, SW | - |
dc.identifier.scopusid | 2-s2.0-84866177483 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 20 | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | T-CELLS | - |
dc.subject.keywordPlus | IMMUNE REGULATION | - |
dc.subject.keywordPlus | VITAMIN-A | - |
dc.subject.keywordPlus | ACID | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | RESPONSES | - |
dc.subject.keywordPlus | MICROBIOTA | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | SYSTEM | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
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