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Transcription factor KLF10 constrains IL-17-committed Vγ4+ γδ T cells

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dc.contributor.authorGirak Kim-
dc.contributor.authorMin Jeong Gu-
dc.contributor.authorSoo Ji Kim-
dc.contributor.authorKwang Hyun Ko-
dc.contributor.authorYoon-Chul Kye-
dc.contributor.authorCheol Gyun Kim-
dc.contributor.authorJae-Ho Cho-
dc.contributor.authorWoon-Kyu Lee-
dc.contributor.authorKi-Duk Song-
dc.contributor.authorHyuk Chu-
dc.contributor.authorYeong-Min Park-
dc.contributor.authorSeung Hyun Han-
dc.contributor.authorCheol-Heui Yun-
dc.date.available2018-07-18T02:06:22Z-
dc.date.created2018-03-15-
dc.date.issued2018-02-
dc.identifier.issn1664-3224-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/4683-
dc.description.abstractγδ T cells, known to be an important source of innate IL-17 in mice, provide critical contributions to host immune responses. Development and function of γδ T cells are directed by networks of diverse transcription factors (TFs). Here, we examine the role of the zinc finger TFs, Kruppel-like factor 10 (KLF10), in the regulation of IL-17-committed CD27- γδ T (γδ27--17) cells. We found selective augmentation of Vγ4+ γδ27- cells with higher IL-17 production in KLF10-deficient mice. Surprisingly, KLF10-deficient CD127hi Vγ4+ γδ27--17 cells expressed higher levels of CD5 than their wild-type counterparts, with hyper-responsiveness to cytokine, but not T-cell receptor, stimuli. Thymic maturation of Vγ4+ γδ27- cells was enhanced in newborn mice deficient in KLF10. Finally, a mixed bone marrow chimera study indicates that intrinsic KLF10 signaling is requisite to limit Vγ4+ γδ27--17 cells. Collectively, these findings demonstrate that KLF10 regulates thymic development of Vγ4+ γδ27- cells and their peripheral homeostasis at steady state. © 2018 Kim, Gu, Kim, Ko, Kye, Kim, Cho, Lee, Song, Chu, Park, Han and Yun-
dc.description.uri1-
dc.formatapplication/pdf-
dc.language영어-
dc.publisherFRONTIERS MEDIA SA-
dc.subjectHomeostasis-
dc.subjectIL-17-
dc.subjectInnate-like γδ-17-
dc.subjectKLF10-
dc.subjectγδ T cells-
dc.titleTranscription factor KLF10 constrains IL-17-committed Vγ4+ γδ T cells-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000426287700001-
dc.identifier.scopusid2-s2.0-85042717929-
dc.identifier.rimsid63047-
dc.contributor.affiliatedAuthorJae-Ho Cho-
dc.identifier.doi10.3389/fimmu.2018.00196-
dc.identifier.bibliographicCitationFRONTIERS IN IMMUNOLOGY, v.9, no.196, pp.1 - 15-
dc.citation.titleFRONTIERS IN IMMUNOLOGY-
dc.citation.volume9-
dc.citation.number196-
dc.citation.startPage1-
dc.citation.endPage15-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordAuthorHomeostasis-
dc.subject.keywordAuthorIL-17-
dc.subject.keywordAuthorInnate-like γδ-17-
dc.subject.keywordAuthorKLF10-
dc.subject.keywordAuthorγδ T cells-
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Academy of Immunology and Microbiology(면역 미생물 공생 연구단) > 1. Journal Papers (저널논문)
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