A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy

Membranous nephropathy (MN) is an organ-restricted autoimmune disease mainly caused by circulating autoantibodies against podocyte antigens, including the M-type phospholipase A2 receptor (PLA2R) and thrombospondin domain-containing 7A (THSD7A). Antibodies against PLA2R are present in 70%–80% and ag...

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Main Authors: Pingna Zhang, Weijun Huang, Qiyan Zheng, Jingyi Tang, Zhaocheng Dong, Yuhua Jiang, Yuning Liu, Weijing Liu
Format: Article
Language:English
Published: Wiley 2021-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2021/8163298
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author Pingna Zhang
Weijun Huang
Qiyan Zheng
Jingyi Tang
Zhaocheng Dong
Yuhua Jiang
Yuning Liu
Weijing Liu
author_facet Pingna Zhang
Weijun Huang
Qiyan Zheng
Jingyi Tang
Zhaocheng Dong
Yuhua Jiang
Yuning Liu
Weijing Liu
author_sort Pingna Zhang
collection DOAJ
description Membranous nephropathy (MN) is an organ-restricted autoimmune disease mainly caused by circulating autoantibodies against podocyte antigens, including the M-type phospholipase A2 receptor (PLA2R) and thrombospondin domain-containing 7A (THSD7A). Antibodies against PLA2R are present in 70%–80% and against THSD7A in 2% of adult patients, which provides a paradigm shift in molecular diagnosis and management monitoring. Both antigens share some similar characteristics: they are expressed by podocytes and have wide tissue distributions; they are bound by autoantibodies only under nonreducing conditions, and the subtype of most autoantibodies is IgG4. However, the factors triggering autoantibody production as well as the association among air pollution, malignancy, and the pathogenesis of MN remain unclear. In this review, we discuss the similarity between the pathological mechanisms triggered by disparate antigens and their associated diseases. Furthermore, we demonstrated the possibility that PM2.5, malignancy, and gene expression specifically induce exposure of these antigens through conformational changes, molecular mimicry, or increased expression eliciting autoimmune responses. Thus, this review provides novel insights into the pathological mechanism of MN.
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institution Kabale University
issn 2314-8861
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language English
publishDate 2021-01-01
publisher Wiley
record_format Article
series Journal of Immunology Research
spelling doaj-art-375352031bdc4d8ea236a0e27694b9262025-02-03T01:25:48ZengWileyJournal of Immunology Research2314-88612314-71562021-01-01202110.1155/2021/81632988163298A Novel Insight into the Role of PLA2R and THSD7A in Membranous NephropathyPingna Zhang0Weijun Huang1Qiyan Zheng2Jingyi Tang3Zhaocheng Dong4Yuhua Jiang5Yuning Liu6Weijing Liu7Renal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaKey Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, ChinaRenal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaRenal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaRenal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaRenal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaRenal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaRenal Research Institution of Beijing University of Chinese Medicine, Beijing, ChinaMembranous nephropathy (MN) is an organ-restricted autoimmune disease mainly caused by circulating autoantibodies against podocyte antigens, including the M-type phospholipase A2 receptor (PLA2R) and thrombospondin domain-containing 7A (THSD7A). Antibodies against PLA2R are present in 70%–80% and against THSD7A in 2% of adult patients, which provides a paradigm shift in molecular diagnosis and management monitoring. Both antigens share some similar characteristics: they are expressed by podocytes and have wide tissue distributions; they are bound by autoantibodies only under nonreducing conditions, and the subtype of most autoantibodies is IgG4. However, the factors triggering autoantibody production as well as the association among air pollution, malignancy, and the pathogenesis of MN remain unclear. In this review, we discuss the similarity between the pathological mechanisms triggered by disparate antigens and their associated diseases. Furthermore, we demonstrated the possibility that PM2.5, malignancy, and gene expression specifically induce exposure of these antigens through conformational changes, molecular mimicry, or increased expression eliciting autoimmune responses. Thus, this review provides novel insights into the pathological mechanism of MN.http://dx.doi.org/10.1155/2021/8163298
spellingShingle Pingna Zhang
Weijun Huang
Qiyan Zheng
Jingyi Tang
Zhaocheng Dong
Yuhua Jiang
Yuning Liu
Weijing Liu
A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy
Journal of Immunology Research
title A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy
title_full A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy
title_fullStr A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy
title_full_unstemmed A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy
title_short A Novel Insight into the Role of PLA2R and THSD7A in Membranous Nephropathy
title_sort novel insight into the role of pla2r and thsd7a in membranous nephropathy
url http://dx.doi.org/10.1155/2021/8163298
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