Goto M, Okamoto M, Sasano M, Nishizawa K, Aotsuka S, Yamaguchi N, Obinata M, Ikeda K
Division of Rheumatic Diseases, Tokyo Metropolitan Otsuka Hospital, Japan.
Clin Exp Immunol. 1991 Dec;86(3):387-92. doi: 10.1111/j.1365-2249.1991.tb02942.x.
A total of 14 transformed cell clones were obtained by micro-injecting origin-defective SV40 DNA into three types of cloned adherent synovial cells (ASC) (dendritic cells (DCs), macrophage-like cells (MCs), and fibroblast-like cells (FCs)) from two rheumatoid arthritis patients (five DC clones (SV40-DCs), five MC clones (SV40-MCs) and four FC clones (SV40-FCs)). All the transformed cell nuclei expressed SV40-specific T antigen. The cells which formed a colony had a few times shorter doubling time than the original cells. IL-1 alpha, IL-1 beta and prostaglandin E2 were detected in the culture supernatant from the unstimulated transformed cells like untransformed cells. The SV40-DCs showed the most potent accessory cell function in oxidative mitogenesis assay among the three types of SV40-ASCs. Granulocyte macrophage colony stimulatory factor (GM-CSF) was detected only in the culture supernatant from the SV40-MCs without stimulation. Extensive phenotypic analysis revealed relatively cell-specific markers. SV40-DCs were HLA-DP+ and glial fibrillary acidic protein positive. SV40-MCs stained positive for 5'-nucleotidase and nonspecific esterase. These transformed ASCs retained much of the original cellular physiology of rheumatoid arthritis (RA) ASCs and may be a useful tool for characterizing the role of ASCs in the pathogenesis of RA.
通过将起源缺陷型SV40 DNA显微注射到两名类风湿性关节炎患者的三种克隆贴壁滑膜细胞(ASC)(树突状细胞(DC)、巨噬细胞样细胞(MC)和成纤维细胞样细胞(FC))中,共获得了14个转化细胞克隆(五个DC克隆(SV40-DC)、五个MC克隆(SV40-MC)和四个FC克隆(SV40-FC))。所有转化细胞核均表达SV40特异性T抗原。形成集落的细胞倍增时间比原始细胞短几倍。与未转化细胞一样,在未刺激的转化细胞培养上清液中检测到IL-1α、IL-1β和前列腺素E2。在三种类型的SV40-ASC中,SV40-DC在氧化有丝分裂试验中表现出最强的辅助细胞功能。仅在未刺激的SV40-MC培养上清液中检测到粒细胞巨噬细胞集落刺激因子(GM-CSF)。广泛的表型分析揭示了相对细胞特异性的标志物。SV40-DC为HLA-DP+且胶质纤维酸性蛋白呈阳性。SV40-MC对5'-核苷酸酶和非特异性酯酶染色呈阳性。这些转化的ASC保留了类风湿性关节炎(RA)ASC的许多原始细胞生理学特性,可能是表征ASC在RA发病机制中作用的有用工具。