0 118

Cited 9 times in

Atherogenic dyslipidemia promotes autoimmune follicular helper T cell responses via IL-27.

DC FieldValueLanguage
dc.contributor.author이상학-
dc.date.accessioned2018-10-11T08:57:18Z-
dc.date.available2018-10-11T08:57:18Z-
dc.date.issued2018-
dc.identifier.issn1529-2908-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/163498-
dc.description.abstractThe incidence of atherosclerosis is higher among patients with systemic lupus erythematosus (SLE); however, the mechanism by which an atherogenic environment affects autoimmunity remains unclear. We found that reconstitution of atherosclerosis-prone Apoe-/- and Ldlr-/- mice with bone marrow from lupus-prone BXD2 mice resulted in increased autoantibody production and glomerulonephritis. This enhanced disease was associated with an increase in CXCR3+ follicular helper T cells (TFH cells). TFH cells isolated from Apoe-/- mice had higher expression of genes associated with inflammatory responses and SLE and were more potent in inducing production of the immunoglobulin IgG2c. Mechanistically, the atherogenic environment induced the cytokine IL-27 from dendritic cells in a Toll-like receptor 4 (TLR4)-dependent manner, which in turn triggered the differentiation of CXCR3+ TFH cells while inhibiting the differentiation of follicular regulatory T cells. Blockade of IL-27 signals diminished the increased TFH cell responses in atherogenic mice. Thus, atherogenic dyslipidemia augments autoimmune TFH cell responses and subsequent IgG2c production in a TLR4- and IL-27-dependent manner.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherNature America Inc.-
dc.relation.isPartOfNATURE IMMUNOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleAtherogenic dyslipidemia promotes autoimmune follicular helper T cell responses via IL-27.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Internal Medicine-
dc.contributor.googleauthorHeeju Ryu-
dc.contributor.googleauthorHoyong Lim-
dc.contributor.googleauthorGaram Choi-
dc.contributor.googleauthorYoung-Jun Park-
dc.contributor.googleauthorMinkyoung Cho-
dc.contributor.googleauthorHyeongjin Na-
dc.contributor.googleauthorChul Won Ahn-
dc.contributor.googleauthorYoung Chul Kim-
dc.contributor.googleauthorWan-Uk Kim-
dc.contributor.googleauthorSang-Hak Lee-
dc.contributor.googleauthorYeonseok Chung-
dc.identifier.doi10.1038/s41590-018-0102-6-
dc.contributor.localIdA02833-
dc.relation.journalcodeJ03205-
dc.identifier.eissn1529-2916-
dc.identifier.pmid29713015-
dc.contributor.alternativeNameLee, Snag Hak-
dc.contributor.affiliatedAuthorLee, Snag Hak-
dc.citation.volume19-
dc.citation.startPage583-
dc.citation.endPage593-
dc.identifier.bibliographicCitationNATURE IMMUNOLOGY, Vol.19 : 583-593, 2018-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.