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深入了解人类氨酰-tRNA合成酶作为特发性炎性肌病中的自身抗原。

Comprehensive insight into human aminoacyl-tRNA synthetases as autoantigens in idiopathic inflammatory myopathies.

作者信息

Jura Miroslawa, Rychlewski Leszek, Barciszewski Jan

机构信息

Institute of Bioorganic Chemistry, Polish Academy of Sciences, 60-704 Poznan, Poland.

出版信息

Crit Rev Immunol. 2007;27(6):559-72. doi: 10.1615/critrevimmunol.v27.i6.60.

DOI:10.1615/critrevimmunol.v27.i6.60
PMID:18197801
Abstract

Autoantibodies against aminoacyl-tRNA synthetases (anti-AARS) belong to the group of the myositis specific autoantibodies (MSAs). Their association with the onset and development of the idiopathic inflammatory myopathies (IIM) implies their participation in the pathogenesis of the diseases. Since the appearing of anti-Jo-1 and other anti-AARSs is related to characteristic immunogenetic and clinical features, they can be considered specific markers in diagnosis and classification of patients affected by IIM. Here, we present an overview of anti-AARSs, their chemoattractant properties, their detection methods, genetic risks, and protective factors.

摘要

抗氨酰-tRNA合成酶自身抗体(抗AARS)属于肌炎特异性自身抗体(MSA)组。它们与特发性炎性肌病(IIM)的发病和发展相关,这意味着它们参与了疾病的发病机制。由于抗Jo-1和其他抗AARS的出现与特征性免疫遗传和临床特征有关,它们可被视为IIM患者诊断和分类的特异性标志物。在此,我们概述了抗AARS、它们的趋化特性、检测方法、遗传风险和保护因素。

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J Biol Chem. 2014 Jul 11;289(28):19269-75. doi: 10.1074/jbc.C114.571026. Epub 2014 Jun 4.
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Internally deleted human tRNA synthetase suggests evolutionary pressure for repurposing.内部缺失的人 tRNA 合成酶提示了重新用途的进化压力。
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