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

Authors
 Heeju Ryu  ;  Hoyong Lim  ;  Garam Choi  ;  Young-Jun Park  ;  Minkyoung Cho  ;  Hyeongjin Na  ;  Chul Won Ahn  ;  Young Chul Kim  ;  Wan-Uk Kim  ;  Sang-Hak Lee  ;  Yeonseok Chung 
Citation
 Nature Immunology, Vol.19 : 583-593, 2018 
Journal Title
 Nature Immunology 
ISSN
 1529-2908 
Issue Date
2018
Abstract
The 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.
DOI
10.1038/s41590-018-0102-6
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실)
Yonsei Authors
이상학(Lee, Sang Hak) ORCID logo https://orcid.org/0000-0002-4535-3745
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/163498
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