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Dendritic Cells Induce a Subpopulation of IL-12Rβ2-Expressing Treg that Specifically Consumes IL-12 to Control Th1 Responses

DC FieldValueLanguage
dc.contributor.author박채규-
dc.date.accessioned2017-02-24T03:17:12Z-
dc.date.available2017-02-24T03:17:12Z-
dc.date.issued2016-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/146300-
dc.description.abstractCytokines secreted from dendritic cells (DCs) play an important role in the regulation of T helper (Th) cell differentiation and activation into effector cells. Therefore, controlling cytokine secretion from DCs may potentially regulate Th differentiation/activation. DCs also induce de-novo generation of regulatory T cells (Treg) that modulate the immune response. In the current study we used the mixed leukocyte reaction (MLR) to investigate the effect of allospecific Treg on IL-12, TNFα and IL-6 secretion by DCs. Treg cells were found to markedly down-regulate IL-12 secretion from DCs following stimulation with TLR7/8 agonist. This down-regulation of IL-12 was neither due to a direct suppression of its production by the DCs nor a result of marked DC death. We found that IL-12 was rather actively consumed by Treg cells. IL-12 consumption was mediated by a subpopulation of IL-12Rβ2-expressing Treg cells and was dependent on MHC class-II expressed on dendritic cells. Furthermore, IL-12 consumption by Tregs increased their suppressive effect on T cell proliferation and Th1 activation. These results provide a new pathway of Th1 response regulation where IL-12 secreted by DCs is consumed by a sub-population of IL-12Rβ2-expressing Treg cells. Consumption of IL-12 by Tregs not only reduces the availability of IL-12 to Th effector cells but also enhances the Treg immunosuppressive effect. This DC-induced IL-12Rβ2-expressing Treg subpopulation may have a therapeutic advantage in suppressing Th1 mediated autoimmunity.-
dc.description.statementOfResponsibilityopen-
dc.format.extente0146412-
dc.languageEnglish-
dc.publisherPublic Library of Science-
dc.relation.isPartOfPLOS ONE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHBiological Transport-
dc.subject.MESHCell Differentiation-
dc.subject.MESHCell Lineage/genetics-
dc.subject.MESHCell Lineage/immunology*-
dc.subject.MESHCell Proliferation-
dc.subject.MESHDendritic Cells/cytology*-
dc.subject.MESHDendritic Cells/immunology-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHImmunophenotyping-
dc.subject.MESHInterleukin-12/genetics*-
dc.subject.MESHInterleukin-12/immunology-
dc.subject.MESHInterleukin-6/genetics-
dc.subject.MESHInterleukin-6/immunology-
dc.subject.MESHLymphocyte Culture Test, Mixed-
dc.subject.MESHMembrane Glycoproteins/genetics-
dc.subject.MESHMembrane Glycoproteins/immunology-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred BALB C-
dc.subject.MESHReceptors, Interleukin-12/genetics*-
dc.subject.MESHReceptors, Interleukin-12/immunology-
dc.subject.MESHSignal Transduction-
dc.subject.MESHT-Lymphocytes, Regulatory/cytology*-
dc.subject.MESHT-Lymphocytes, Regulatory/immunology-
dc.subject.MESHTh1 Cells/cytology*-
dc.subject.MESHTh1 Cells/immunology-
dc.subject.MESHTh1-Th2 Balance-
dc.subject.MESHToll-Like Receptor 7/genetics-
dc.subject.MESHToll-Like Receptor 7/immunology-
dc.subject.MESHToll-Like Receptor 8/genetics-
dc.subject.MESHToll-Like Receptor 8/immunology-
dc.subject.MESHTumor Necrosis Factor-alpha/genetics-
dc.subject.MESHTumor Necrosis Factor-alpha/immunology-
dc.titleDendritic Cells Induce a Subpopulation of IL-12Rβ2-Expressing Treg that Specifically Consumes IL-12 to Control Th1 Responses-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Life Science-
dc.contributor.googleauthorUri Sela-
dc.contributor.googleauthorChae Gyu Park-
dc.contributor.googleauthorAndrew Park-
dc.contributor.googleauthorPeter Olds-
dc.contributor.googleauthorShu Wang-
dc.contributor.googleauthorRalph M. Steinman-
dc.contributor.googleauthorVincent A. Fischetti-
dc.identifier.doi10.1371/journal.pone.0146412-
dc.contributor.localIdA01718-
dc.relation.journalcodeJ02540-
dc.identifier.eissn1932-6203-
dc.identifier.pmid26745371-
dc.contributor.alternativeNamePark, Chae Gyu-
dc.contributor.affiliatedAuthorPark, Chae Gyu-
dc.citation.volume11-
dc.citation.number1-
dc.citation.startPagee0146412-
dc.identifier.bibliographicCitationPLOS ONE, Vol.11(1) : e0146412, 2016-
dc.date.modified2017-02-24-
dc.identifier.rimsid53030-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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