Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 윤지희 | - |
dc.date.accessioned | 2019-12-03T01:31:27Z | - |
dc.date.available | 2019-12-03T01:31:27Z | - |
dc.date.issued | 2017-12 | - |
dc.identifier.citation | FRONTIERS IN IMMUNOLOGY, v. 8, Article no. 1793 | en_US |
dc.identifier.issn | 1664-3224 | - |
dc.identifier.uri | https://www.frontiersin.org/articles/10.3389/fimmu.2017.01793/full | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/116644 | - |
dc.description.abstract | Dysfunction of T helper 17 (Th17) cells leads to chronic inflammatory disorders. Signal transducer and activator of transcription 3 (STAT3) orchestrates the expression of proinflammatory cytokines and pathogenic cell differentiation from interleukin (IL)-17-producing Th17 cells. However, the pathways mediated by STAT3 signaling are not fully understood. Here, we observed that Fos-related antigen 1 (FRA1) and JUNB are directly involved in STAT3 binding to sites in the promoters of Fosl1 and Junb. Promoter binding increased expression of IL-17 and the development of Th17 cells. Overexpression of Fra1 and Junb in mice resulted in susceptibility to collagen-induced arthritis and an increase in Th17 cell numbers and inflammatory cytokine production. In patients with rheumatoid arthritis, FRA1 and JUNB were colocalized with STAT3 in the inflamed synovium. These observations suggest that FRA1 and JUNB are associated closely with STAT3 activation, and that this activation leads to Th17 cell differentiation in autoimmune diseases and inflammation. | en_US |
dc.description.sponsorship | This study was supported by a grant of the Korean Health Technology R&D Project, Ministry for Health & Welfare, Republic of Korea (grant no. HI14C3417), by the Basic Science Research Program from the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (grant no. 2012-0006135), and by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, funded by the Ministry of Health & Welfare, Republic of Korea (grant no. HI15C3062). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | FRONTIERS MEDIA SA | en_US |
dc.subject | Fos-related antigen 1-JUNB | en_US |
dc.subject | signal transducer and activator of transcription 3 | en_US |
dc.subject | T helper 17 | en_US |
dc.subject | autoimmune arthritis | en_US |
dc.subject | inflammation | en_US |
dc.title | The Fos-related antigen 1-JUnB/activator Protein 1 Transcription complex, a Downstream Target of signal Transducer and activator of Transcription 3, induces T helper 17 Differentiation and Promotes experimental autoimmune arthritis | en_US |
dc.type | Article | en_US |
dc.relation.volume | 8 | - |
dc.identifier.doi | 10.3389/fimmu.2017.01793 | - |
dc.relation.page | 1-11 | - |
dc.relation.journal | FRONTIERS IN IMMUNOLOGY | - |
dc.contributor.googleauthor | Moon, Young-Mee | - |
dc.contributor.googleauthor | Lee, Seon-Yeong | - |
dc.contributor.googleauthor | Kwok, Seung-Ki | - |
dc.contributor.googleauthor | Lee, Seung Hoon | - |
dc.contributor.googleauthor | Kim, Deokhoon | - |
dc.contributor.googleauthor | Kim, Woo Kyung | - |
dc.contributor.googleauthor | Her, Yang-Mi | - |
dc.contributor.googleauthor | Son, Hea-Jin | - |
dc.contributor.googleauthor | Kim, Eun-Kyung | - |
dc.contributor.googleauthor | Youn, Jeehee | - |
dc.relation.code | 2017006900 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jhyoun | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.