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人I型嗜T细胞病毒感染的淋巴细胞在病毒诱导的关节病病变中的寡克隆增殖。

Oligoclonal proliferation of human T-cell leukemia virus type I infected lymphocytes in lesions of virus-induced arthropathy.

作者信息

Yamamoto K, Aono H, Nakajima T, Hasunuma T, Nishioka K

机构信息

Division of Rheumatology and Molecular Immunology, St. Marianna University School of Medicine, Kawasaki, Japan.

出版信息

Biochem Biophys Res Commun. 1995 Mar 28;208(3):1040-5. doi: 10.1006/bbrc.1995.1439.

Abstract

To investigate the pathogenesis of human T-cell leukemia virus type I associated arthropathy, the mode of proviral integration in the pathological lesions was analyzed using ligation-mediated polymerase chain reaction. Peripheral blood mononuclear cells (PBMC) of these patients possessed multiple dominant clones of the virus-infected cells. On the other hand, synovial fluid cells of the affected joints exhibited fewer dominant clones even though the copy numbers of the provirus were comparable to those of PBMC. Thus, restricted HTLV-I infected T cell clones may proliferate and expand in the lesions.

摘要

为研究I型人类T细胞白血病病毒相关性关节病的发病机制,利用连接介导的聚合酶链反应分析了病理病变中前病毒的整合模式。这些患者的外周血单个核细胞(PBMC)拥有多个病毒感染细胞的优势克隆。另一方面,尽管前病毒的拷贝数与PBMC相当,但受累关节的滑液细胞显示出较少的优势克隆。因此,受限的HTLV-I感染T细胞克隆可能在病变中增殖和扩增。

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