Center for Autoimmune Diseases, Rheumatology Unit, Sheba Medical Center (SMC), Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Autoimmunity. 2009 Aug;42(5):432-8. doi: 10.1080/08916930802613210.
Infectious agents have been implicated in the etiopathogenesis of various vasculitides via numerous and overlapping mechanisms including direct microbial invasion of endothelial cells, immune complex mediated vessel wall damage and stimulation of autoreactive B and/or T cells through molecular mimicry and superantigens. While the causative role of hepatitis B virus in polyarteritis nodosa and hepatitis C virus in mixed cryoglobulinemia is clearly established, evidence for the association of other infectious agents with vasculitis, including human immunodeficiency virus, parvovirus B19, cytomegalovirus, varicella zoster virus, Staphylococcus aureus, rickettsiaceae, Treponema pallidum and Borrelia burgdorferi, among numerous others, is accumulating. The spectrum of association of infectious agents; bacteria, viruses and parasites, with systemic vasculitides, will be reviewed herewith.
传染因子通过多种重叠机制与各种血管炎的病因发病机制有关,包括直接侵犯内皮细胞、免疫复合物介导的血管壁损伤以及分子模拟和超抗原刺激自身反应性 B 和/或 T 细胞。虽然乙型肝炎病毒在结节性多动脉炎和丙型肝炎病毒在混合性冷球蛋白血症中的致病作用已明确确立,但其他传染因子与血管炎的关联证据也在不断增加,包括人类免疫缺陷病毒、细小病毒 B19、巨细胞病毒、水痘带状疱疹病毒、金黄色葡萄球菌、立克次体、苍白密螺旋体和伯氏疏螺旋体等。本文将对传染因子(细菌、病毒和寄生虫)与系统性血管炎的关联进行综述。