Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice
Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were gener...
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2021
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oai:doaj.org-article:527c6365fe894cf79ff097e3b7400ebd2021-12-02T16:27:45ZOverexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice10.1038/s41598-021-94855-52045-2322https://doaj.org/article/527c6365fe894cf79ff097e3b7400ebd2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94855-5https://doaj.org/toc/2045-2322Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.Jinhee LeeSoyoung JangMinjee ChoiMincheol KangSu-Geun LimSI-Yong KimSoyeon JangJiwon KoEungyung KimJunkoo YiYeonsik ChooMyoung Ok KimZae Young RyooNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-8 (2021) |
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Medicine R Science Q Jinhee Lee Soyoung Jang Minjee Choi Mincheol Kang Su-Geun Lim SI-Yong Kim Soyeon Jang Jiwon Ko Eungyung Kim Junkoo Yi Yeonsik Choo Myoung Ok Kim Zae Young Ryoo Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice |
description |
Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms. |
format |
article |
author |
Jinhee Lee Soyoung Jang Minjee Choi Mincheol Kang Su-Geun Lim SI-Yong Kim Soyeon Jang Jiwon Ko Eungyung Kim Junkoo Yi Yeonsik Choo Myoung Ok Kim Zae Young Ryoo |
author_facet |
Jinhee Lee Soyoung Jang Minjee Choi Mincheol Kang Su-Geun Lim SI-Yong Kim Soyeon Jang Jiwon Ko Eungyung Kim Junkoo Yi Yeonsik Choo Myoung Ok Kim Zae Young Ryoo |
author_sort |
Jinhee Lee |
title |
Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice |
title_short |
Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice |
title_full |
Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice |
title_fullStr |
Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice |
title_full_unstemmed |
Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice |
title_sort |
overexpression of cathepsin s exacerbates lupus pathogenesis through upregulation tlr7 and ifn-α in transgenic mice |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/527c6365fe894cf79ff097e3b7400ebd |
work_keys_str_mv |
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