期刊
CELL STRESS & CHAPERONES
卷 25, 期 5, 页码 737-741出版社
SPRINGER
DOI: 10.1007/s12192-020-01148-3
关键词
Severe acute respiratory syndrome coronavirus 2; COVID-19; Molecular chaperones; Molecular mimicry; Autoimmunity; Endothelialitis
类别
资金
- University of Palermo
- Universite PSL
- Centre de Recherche Inria de Paris
- Universite de Lyon
- IMET
- IEMEST
Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of COVID-19 disease, has the potential to elicit autoimmunity because mimicry of human molecular chaperones by viral proteins. We compared viral proteins with human molecular chaperones, many of which are heat shock proteins, to determine if they share amino acid-sequence segments with immunogenic-antigenic potential, which can elicit cross-reactive antibodies and effector immune cells with the capacity to damage-destroy human cells by a mechanism of autoimmunity. We identified the chaperones that can putatively participate in molecular mimicry phenomena after SARS-CoV-2 infection, focusing on those for which endothelial cell plasma-cell membrane localization has already been demonstrated. We also postulate that post-translational modifications, induced by physical (shear) and chemical (metabolic) stress caused respectively by the risk factors hypertension and diabetes, might have a role in determining plasma-cell membrane localization and, in turn, autoimmune-induced endothelial damage.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据