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DC Field | Value | Language |
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dc.citation.endPage | 10195 | - |
dc.citation.number | 38 | - |
dc.citation.startPage | 10190 | - |
dc.citation.title | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | - |
dc.citation.volume | 114 | - |
dc.contributor.author | Do, Jeongsu | - |
dc.contributor.author | Kim, Dongkyun | - |
dc.contributor.author | Kim, Sohee | - |
dc.contributor.author | Valentin-Torres, Alice | - |
dc.contributor.author | Dvorina, Nina | - |
dc.contributor.author | Jang, Eunjung | - |
dc.contributor.author | Nagarajavel, Vivekananthan | - |
dc.contributor.author | DeSilva, Tara M. | - |
dc.contributor.author | Li, Xiaoxia | - |
dc.contributor.author | Ting, Angela H. | - |
dc.contributor.author | Vignali, Dario A. A. | - |
dc.contributor.author | Stohlman, Stephen A. | - |
dc.contributor.author | Baldwin, William M., III | - |
dc.contributor.author | Min, Booki | - |
dc.date.accessioned | 2023-12-21T21:45:32Z | - |
dc.date.available | 2023-12-21T21:45:32Z | - |
dc.date.created | 2017-10-10 | - |
dc.date.issued | 2017-09 | - |
dc.description.abstract | Dysregulated Foxp3(+) Treg functions result in uncontrolled immune activation and autoimmunity. Therefore, identifying cellular factors modulating Treg functions is an area of great importance. Here, using Treg-specific Il27ra(-/-) mice, we report that IL-27 signaling in Foxp3(+) Tregs is essential for Tregs to control autoimmune inflammation in the central nervous system (CNS). Following experimental autoimmune encephalomyelitis (EAE) induction, Treg-specific Il27ra-/- mice develop more severe EAE. Consistent with the severe disease, the numbers of IFN gamma- and IL-17-producing CD4 T cells infiltrating the CNS tissues are greater in these mice. Treg accumulation in the inflamed CNS tissues is not affected by the lack of IL-27 signaling in Tregs, suggesting a functional defect of Il27ra(-/-) Tregs. IL-10 production by conventional CD4 T cells and their CNS accumulation are rather elevated in Treg-specific Il27ra(-/-) mice. Analysis with Treg fate-mapping reporter mice further demonstrates that IL-27 signaling in Tregs may control stability of Foxp3 expression. Finally, systemic administration of recombinant IL-27 in Treg-specific Il27ra(-/-) mice fails to ameliorate the disease even in the presence of IL-27-responsive conventional CD4 T cells. These findings uncover a previously unknown role of IL-27 in regulating Treg function to control autoimmune inflammation. | - |
dc.identifier.bibliographicCitation | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.114, no.38, pp.10190 - 10195 | - |
dc.identifier.doi | 10.1073/pnas.1703100114 | - |
dc.identifier.issn | 0027-8424 | - |
dc.identifier.scopusid | 2-s2.0-85029569999 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/22776 | - |
dc.identifier.url | http://www.pnas.org/content/114/38/10190 | - |
dc.identifier.wosid | 000411157100070 | - |
dc.language | 영어 | - |
dc.publisher | NATL ACAD SCIENCES | - |
dc.title | Treg-specific IL-27R alpha deletion uncovers a key role for IL-27 in Treg function to control autoimmunity | - |
dc.type | Article | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | autoimmunity | - |
dc.subject.keywordAuthor | Foxp3+regulatory T cells | - |
dc.subject.keywordAuthor | IL-27 | - |
dc.subject.keywordAuthor | Tr1 cells | - |
dc.subject.keywordPlus | REGULATORY T-CELLS | - |
dc.subject.keywordPlus | CENTRAL-NERVOUS-SYSTEM | - |
dc.subject.keywordPlus | DENDRITIC CELLS | - |
dc.subject.keywordPlus | TH17 CELLS | - |
dc.subject.keywordPlus | MULTIPLE-SCLEROSIS | - |
dc.subject.keywordPlus | SUPPRESSION | - |
dc.subject.keywordPlus | INTERLEUKIN-27 | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | ENCEPHALOMYELITIS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
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