Randone Silvia Bellando, Guiducci Serena, Cerinic Marco Matucci
Department of Biomedicine, DENOThe Centre, Division of Rheumatology AOUC, University of Florence, Florence, Italy.
Autoimmun Rev. 2008 Oct;8(1):36-40. doi: 10.1016/j.autrev.2008.07.022. Epub 2008 Aug 13.
Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular obliteration, excessive extracellular matrix deposition and fibrosis of the connective tissues of the skin, lungs, gastrointestinal tract, heart, and kidneys. Numerous infectious agents (bacterial and viral) have been proposed as possible triggering factors (Parvovirus B19, Cytomegalovirus, Epstein-Barr virus, Retroviruses). Homology between viruses and autoantibody targets suggests that molecular mimicry may have a role in initiating antibody response in different disorders characterized by diffuse vascular disease, including SSc. Endothelial cell may be infected bacteria or viruses that play a particular role in inducing vasculitis. The pathogenic hypothesis include: a mechanism of molecular mimicry, the role played by endothelial cell damage, the presence of superantigens and the role of microchimeric cells. Although several studies provide important information linking infectious agents to SSc, a direct casual association between infections and SSc is still missing. In SSc viral products could synergize with other factors in the microenvironment predisposing to SSc development.
系统性硬化症（SSc）是一种自身免疫性疾病，其特征为血管闭塞、细胞外基质过度沉积以及皮肤、肺、胃肠道、心脏和肾脏等结缔组织的纤维化。许多感染因子（细菌和病毒）已被提出可能是触发因素（细小病毒B19、巨细胞病毒、爱泼斯坦-巴尔病毒、逆转录病毒）。病毒与自身抗体靶点之间的同源性表明，分子模拟可能在以弥漫性血管疾病为特征的不同疾病（包括SSc）中引发抗体反应方面发挥作用。内皮细胞可能被细菌或病毒感染，这些细菌或病毒在诱导血管炎中起特定作用。致病假说包括：分子模拟机制、内皮细胞损伤所起的作用、超抗原的存在以及微嵌合细胞的作用。尽管多项研究提供了将感染因子与SSc联系起来的重要信息，但感染与SSc之间的直接因果关联仍然缺失。在SSc中，病毒产物可能与微环境中的其他因素协同作用，易导致SSc的发生。
