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Aberrant expression of cell‐free nucleosomes in dermatomyositis/polymyositis
Author(s) -
Zhong Danli,
Wu Chanyuan,
Bai Jingjing,
Zhao Jiuliang,
Xu Dong,
Li Mengtao,
Wang Qian,
Wang Feifei,
Zeng Xiaofeng
Publication year - 2020
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1111/dth.14460
Subject(s) - dermatomyositis , polymyositis , medicine , biomarker , nucleosome , receiver operating characteristic , myositis , immunology , histone , pathology , biology , biochemistry , gene
Nucleosomes are typically located intracellularly, and extracellular levels of nucleosomes indicated the degree of cell death. We postulated aberrant nucleosomes expression in dermatomyositis (DM) and polymyositis (PM). To assess the aberrant expression of circulating nucleosomes in DM and polymyositis. 76 consecutive DM and PM patients from 1 September 2017 to 31 October 2018 were enrolled in this study, in addition to 20 healthy controls. The levels of circulating nucleosomes, with 16 kinds of detectable myositis‐specific antibodies (MSAs) were detected in IIMs patients using enzyme‐linked immunosorbent assay kit (ELISA). Receiver operating characteristic (ROC) curve analysis was performed for evaluating the ability of this candidate marker for detecting DM/PM. The results showed that the levels of circulating nucleosomes in DM/PM patients were significantly higher than that in normal individuals. Specifically, elevated levels of nucleosomes were associated with MDA5 Ab, ARS, and TIF1γAb. In addition, elevated levels of circulating nucleosomes correlated with skin eruption. This study has evidenced nucleosomes as a potential new biomarker of DM/PM. Aberrant nucleosomes expression occurs in myositis patients and the difference in nucleosomes expression between patients with and without skin eruption is statistically significant. A unique expression profile of elevated serum nucleosomes was detected in DM/PM‐MDA5 Ab(+), ASS, and TIF1γAb(+).