Kopelovich L
Laboratory of Cancer Genetics and Cancer Prevention, Department of Veterans Affairs, Bay Pines, Florida.
Eur Cytokine Netw. 1991 Mar-Apr;2(2):99-106.
In an earlier study, we have demonstrated the conversion of human fibroblasts (HF) to tissue macrophages (TM) by the Snyder-Theilen feline sarcoma virus (ST:(FeSV)) [1]. The present study shows that conversion of cultured HF by the ST:FeSV to TM resulted in the de-novo expression of interleukin-1 alpha, IL-1 beta, interferon-alpha, tumor necrosis factor-alpha, granulocyte-macrophage colony stimulating factor, and CD4. The conversion of HF to TM was also associated with increased expression of non-specific esterases as well as increased amount of ingested lipid material by the TM. Clonotypic and organotypic analyses of cells infected with the ST:FeSV(FeLV) showed a similar degree of conversion to TM among eleven individual clones of skin fibroblasts, and among fibroblasts obtained from eight different organs. These findings bear on the origin (heterogeneity) of TM, the nature of TM-induced cytokines, and the potential role of ST:FeSV-recruited TM during immune reactions in vivo.
在一项早期研究中,我们已证明通过斯奈德-泰伦猫肉瘤病毒(ST:(FeSV))可将人成纤维细胞(HF)转化为组织巨噬细胞(TM)[1]。本研究表明,经ST:FeSV将培养的HF转化为TM会导致白细胞介素-1α、IL-1β、干扰素-α、肿瘤坏死因子-α、粒细胞-巨噬细胞集落刺激因子和CD4的从头表达。HF向TM的转化还与非特异性酯酶表达增加以及TM摄取脂质物质的量增加有关。对感染ST:FeSV(FeLV)的细胞进行的克隆型和器官型分析显示,在皮肤成纤维细胞的11个单独克隆以及从8个不同器官获得的成纤维细胞中,向TM的转化程度相似。这些发现与TM的起源(异质性)、TM诱导的细胞因子的性质以及ST:FeSV招募的TM在体内免疫反应中的潜在作用有关。