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Dyslipidemia promotes germinal center reactions via IL-27
Cardiovascular disease such as atherosclerosis is caused by imbalanced lipid metabolism and represents a leading cause of death worldwide. Epidemiological studies show that patients with systemic autoimmune diseases exhibit a higher incidence of atherosclerosis. Conversely, hyperlipidemia has been k...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Society for Biochemistry and Molecular Biology
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6130833/ https://www.ncbi.nlm.nih.gov/pubmed/30037367 http://dx.doi.org/10.5483/BMBRep.2018.51.8.171 |
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author | Ryu, Heeju Chung, Yeonseok |
author_facet | Ryu, Heeju Chung, Yeonseok |
author_sort | Ryu, Heeju |
collection | PubMed |
description | Cardiovascular disease such as atherosclerosis is caused by imbalanced lipid metabolism and represents a leading cause of death worldwide. Epidemiological studies show that patients with systemic autoimmune diseases exhibit a higher incidence of atherosclerosis. Conversely, hyperlipidemia has been known to accelerate the incidence of autoimmune diseases in humans and in animal models. However, there is a considerable gap in our understanding of how atherosclerosis impacts the development of the autoimmunity in humans, and vice versa. The atherosclerosis-related autoimmune diseases include psoriasis, rheumatoid arthritis, systemic lupus erythematosus (SLE) and diabetes mellitus. By using animal models of atherosclerosis and SLE, we have recently demonstrated that hyperlipidemia significantly accelerates the development of autoantibodies, by inducing autoimmune follicular helper T (T(FH)) cells. Mechanistic studies have identified that hyperlipidemia induces IL-27 production in a TLR4-dependent manner, likely via downregulating LXR expression in dendritic cells. In this case, mice lacking IL-27 do not develop enhanced antibody responses. Thus it is noted that these findings propose a mechanistic insight responsible for the tight association between cardiovascular diseases and SLE in humans. |
format | Online Article Text |
id | pubmed-6130833 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Korean Society for Biochemistry and Molecular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-61308332018-09-12 Dyslipidemia promotes germinal center reactions via IL-27 Ryu, Heeju Chung, Yeonseok BMB Rep Perspective Cardiovascular disease such as atherosclerosis is caused by imbalanced lipid metabolism and represents a leading cause of death worldwide. Epidemiological studies show that patients with systemic autoimmune diseases exhibit a higher incidence of atherosclerosis. Conversely, hyperlipidemia has been known to accelerate the incidence of autoimmune diseases in humans and in animal models. However, there is a considerable gap in our understanding of how atherosclerosis impacts the development of the autoimmunity in humans, and vice versa. The atherosclerosis-related autoimmune diseases include psoriasis, rheumatoid arthritis, systemic lupus erythematosus (SLE) and diabetes mellitus. By using animal models of atherosclerosis and SLE, we have recently demonstrated that hyperlipidemia significantly accelerates the development of autoantibodies, by inducing autoimmune follicular helper T (T(FH)) cells. Mechanistic studies have identified that hyperlipidemia induces IL-27 production in a TLR4-dependent manner, likely via downregulating LXR expression in dendritic cells. In this case, mice lacking IL-27 do not develop enhanced antibody responses. Thus it is noted that these findings propose a mechanistic insight responsible for the tight association between cardiovascular diseases and SLE in humans. Korean Society for Biochemistry and Molecular Biology 2018-08 2018-08-31 /pmc/articles/PMC6130833/ /pubmed/30037367 http://dx.doi.org/10.5483/BMBRep.2018.51.8.171 Text en Copyright © 2018 by the The Korean Society for Biochemistry and Molecular Biology This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Perspective Ryu, Heeju Chung, Yeonseok Dyslipidemia promotes germinal center reactions via IL-27 |
title | Dyslipidemia promotes germinal center reactions via IL-27 |
title_full | Dyslipidemia promotes germinal center reactions via IL-27 |
title_fullStr | Dyslipidemia promotes germinal center reactions via IL-27 |
title_full_unstemmed | Dyslipidemia promotes germinal center reactions via IL-27 |
title_short | Dyslipidemia promotes germinal center reactions via IL-27 |
title_sort | dyslipidemia promotes germinal center reactions via il-27 |
topic | Perspective |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6130833/ https://www.ncbi.nlm.nih.gov/pubmed/30037367 http://dx.doi.org/10.5483/BMBRep.2018.51.8.171 |
work_keys_str_mv | AT ryuheeju dyslipidemiapromotesgerminalcenterreactionsviail27 AT chungyeonseok dyslipidemiapromotesgerminalcenterreactionsviail27 |