The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms

Abstract. Psoriasis is a chronic, recurrent, inflammatory skin disease that is often accompanied by obesity. An increasing amount of research has elucidated the pathophysiological link between psoriasis and obesity. Since 2005, interleukin (IL)-17-producing T helper 17 cells and their main effector...

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Main Authors: Cheng Xu, Jie Ji, Ting Su, Hong-Wei Wang, Zhong-Lan Su
Format: Article
Language:English
Published: Wolters Kluwer Health 2021-06-01
Series:International Journal of Dermatology and Venerology
Online Access:http://journals.lww.com/10.1097/JD9.0000000000000155
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spelling doaj-b2cc4ffd29aa4ddf92842210722324e32021-07-26T05:42:20ZengWolters Kluwer HealthInternational Journal of Dermatology and Venerology2096-55402641-87462021-06-014211612110.1097/JD9.0000000000000155202106000-00011The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological MechanismsCheng XuJie JiTing SuHong-Wei WangZhong-Lan SuAbstract. Psoriasis is a chronic, recurrent, inflammatory skin disease that is often accompanied by obesity. An increasing amount of research has elucidated the pathophysiological link between psoriasis and obesity. Since 2005, interleukin (IL)-17-producing T helper 17 cells and their main effector cytokine IL-17A have been considered to play a critical role in the pathogenesis of psoriasis; the marked effect of biotherapies targeting IL-17A on moderate and severe psoriasis has further established its role in psoriasis. Recent studies have found that obesity induces T helper 17 cells to secrete IL-17A and participate in the pathogenesis of psoriasis. IL-17A may be a crucial element in the association between psoriasis and obesity. This review discusses the association between psoriasis and obesity, with a focus on and the implications regarding the need to treat psoriasis.http://journals.lww.com/10.1097/JD9.0000000000000155
collection DOAJ
language English
format Article
sources DOAJ
author Cheng Xu
Jie Ji
Ting Su
Hong-Wei Wang
Zhong-Lan Su
spellingShingle Cheng Xu
Jie Ji
Ting Su
Hong-Wei Wang
Zhong-Lan Su
The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms
International Journal of Dermatology and Venerology
author_facet Cheng Xu
Jie Ji
Ting Su
Hong-Wei Wang
Zhong-Lan Su
author_sort Cheng Xu
title The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms
title_short The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms
title_full The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms
title_fullStr The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms
title_full_unstemmed The Association of Psoriasis and Obesity: Focusing on IL-17A-Related Immunological Mechanisms
title_sort association of psoriasis and obesity: focusing on il-17a-related immunological mechanisms
publisher Wolters Kluwer Health
series International Journal of Dermatology and Venerology
issn 2096-5540
2641-8746
publishDate 2021-06-01
description Abstract. Psoriasis is a chronic, recurrent, inflammatory skin disease that is often accompanied by obesity. An increasing amount of research has elucidated the pathophysiological link between psoriasis and obesity. Since 2005, interleukin (IL)-17-producing T helper 17 cells and their main effector cytokine IL-17A have been considered to play a critical role in the pathogenesis of psoriasis; the marked effect of biotherapies targeting IL-17A on moderate and severe psoriasis has further established its role in psoriasis. Recent studies have found that obesity induces T helper 17 cells to secrete IL-17A and participate in the pathogenesis of psoriasis. IL-17A may be a crucial element in the association between psoriasis and obesity. This review discusses the association between psoriasis and obesity, with a focus on and the implications regarding the need to treat psoriasis.
url http://journals.lww.com/10.1097/JD9.0000000000000155
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