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对接触介导杀伤具有“抗性”或“敏感性”的SV40转化肿瘤细胞的巨噬细胞识别和杀伤特性研究

Characterization of macrophage recognition and killing of SV40-transformed tumor cells that are "resistant" or "susceptible" to contact-mediated killing.

作者信息

Chapes S K, Duffin D, Paulsen A Q

机构信息

Division of Biology, Kansas State University, Manhattan 66506.

出版信息

J Immunol. 1988 Jan 15;140(2):589-96.

PMID:2826595
Abstract

In this report we used the macrophage-"resistant" and -"susceptible" cell lines, F5m and F5b, to determine why AKR or AKR-like virus expression makes the F5m cell line more resistant to in vitro macrophage killing than the F5b cell line. We found that resistance to macrophage killing may be transmitted by an infectious AKR or AKR-like murine leukemia virus and that resistance was concomitant with virus expression as measured by the presence of AKR virus-specific 70 kDa glycoprotein. We report that macrophage cytotoxicity of these cell lines is dependent upon the direct contact between tumor cells and macrophages. In contrast, macrophage-mediated cytostasis occurred via soluble macrophage products and no differential susceptibility of F5b or F5m to macrophage-mediated cytostasis was observed. Macrophage binding of F5b was also significantly better than that of F5m. These data suggest that only the events that depend upon the close contact of macrophages and tumor cells will be affected by the expression of AKR or AKR-like virus. Therefore, the differences in susceptibility of F5m and F5b to direct macrophage-mediated cytotoxicity are apparently because the macrophage binding of F5m is less efficient than the binding of F5b.

摘要

在本报告中,我们使用了巨噬细胞“抗性”和“易感”细胞系F5m和F5b,以确定为何AKR或AKR样病毒的表达会使F5m细胞系比F5b细胞系对体外巨噬细胞杀伤更具抗性。我们发现,对巨噬细胞杀伤的抗性可能由感染性AKR或AKR样鼠白血病病毒传递,并且抗性与通过AKR病毒特异性70 kDa糖蛋白的存在所测量的病毒表达相伴。我们报告说,这些细胞系的巨噬细胞细胞毒性取决于肿瘤细胞与巨噬细胞之间的直接接触。相反,巨噬细胞介导的细胞停滞通过可溶性巨噬细胞产物发生,并且未观察到F5b或F5m对巨噬细胞介导的细胞停滞有不同的敏感性。F5b的巨噬细胞结合也明显优于F5m。这些数据表明,只有依赖于巨噬细胞与肿瘤细胞紧密接触的事件才会受到AKR或AKR样病毒表达的影响。因此,F5m和F5b对直接巨噬细胞介导的细胞毒性的敏感性差异显然是因为F5m的巨噬细胞结合效率低于F5b的结合效率。

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