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[从床边角度看类风湿关节炎的病因/病理生理学/治疗方法]

[Approach from bedside to etiology/pathophysiology/treatment of rheumatoid arthritis].

作者信息

Munakata Yasuhiko

机构信息

Department of Rheumatology and Hematology, Tohoku University Graduate School of Medicine.

出版信息

Nihon Rinsho Meneki Gakkai Kaishi. 2006 Oct;29(5):303-10. doi: 10.2177/jsci.29.303.

DOI:10.2177/jsci.29.303
PMID:17075189
Abstract

Rheumatoid arthritis (RA) is a disease full of variety. We need to elucidate various clinical doubts for the complete cure of RA. We observed a lot of patients with human parvovirus B19 (B19) infection who developed to RA till now. We investigated B19 infection in relation with RA etiology. B19 infects persistently to immune cells through cell surface Ku80 autoantigen as a cellular receptor. We are able to detect B19 in immune cells which infiltrate in synovial tissues of patients with RA. B19 is activated in infected cells, and functional viral protein NS1 induces over production of inflammatory cytokine TNFalpha. As a result, it promotes a neutrophile activation and migration to the synovium where there are B19-infected immune cells. This may cause arthritis and create a vicious circle of chronic inflammation that develops into RA. As for the B19 persistent infection to immune cells, abnormality of anti-B19 humoral immunity may participate in imperfection of B19 neutralization of a host. It is expected the development of effective treatment that cure progressing RA from B19 infection. NS1 may be one of the candidates of therapeutic target.

摘要

类风湿关节炎(RA)是一种具有多样性的疾病。为了彻底治愈RA,我们需要阐明各种临床疑问。到目前为止,我们观察到许多感染人细小病毒B19(B19)的患者发展成了RA。我们研究了与RA病因相关的B19感染情况。B19通过细胞表面的Ku80自身抗原作为细胞受体持续感染免疫细胞。我们能够在浸润于RA患者滑膜组织的免疫细胞中检测到B19。B19在受感染细胞中被激活,功能性病毒蛋白NS1诱导炎性细胞因子TNFα的过度产生。结果,它促进中性粒细胞的活化并迁移至存在被B19感染的免疫细胞的滑膜。这可能导致关节炎并形成慢性炎症的恶性循环,进而发展成RA。至于B19对免疫细胞的持续感染,抗B19体液免疫异常可能参与宿主对B19中和作用的缺陷。有望开发出从B19感染治愈进展性RA的有效治疗方法。NS1可能是治疗靶点的候选之一。

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