MECHANISM OF MACROPHAGE RECOGNITION OF TUMOR CELLS

巨噬细胞被认为是肿瘤监测的重要组成部分 in vivo. 它们被认为是一种极好的肿瘤发生机制 破坏，因为它们会杀死肿瘤细胞，同时留下正常细胞 不受干扰 现在认为巨噬细胞溶解肿瘤细胞的过程 至少有两个可识别的步骤--识别和绑定步骤 随后由巨噬细胞释放细胞毒性介质。 虽然 巨噬细胞细胞毒性的步骤已经被很好地确定， 巨噬细胞用来结合肿瘤的分子或识别结构 细胞或区分正常细胞与肿瘤细胞是未知的。 研究已经分离出了SV 40转化的肿瘤细胞，这些细胞是易感的或 对LPS激活的鼠巨噬细胞的体外细胞溶解具有抗性。 的 特异性RNA肿瘤病毒诱导的gp 70的存在与 对巨噬细胞溶解的抵抗力。 使用Friend白血病病毒 （FLV）转化细胞具有不同的gp 70，与易感细胞相关 巨噬细胞的细胞毒性，而不是巨噬细胞抵抗 发现FLV转化细胞。 研究表明，gp 70可能参与肿瘤识别，但如何 是不确定的。 此外，其他分子的参与 并没有被完全否定。在这项研究中，计划 研究巨噬细胞识别肿瘤细胞的机制， 以生物化学的方式来确定被杀死或未被杀死的细胞之间的差异， 激活的巨噬细胞 （MB）

Macrophages are believed to be an important component of tumor surveillance in vivo. They are thought to be an excellent mechanism of tumor destruction, as they will kill tumor cells while leaving normal cells undisturbed. The process of macrophage lysis of tumor cells is now thought to be at least two identifiable steps--a recognition and binding step followed by the release of cytotoxic mediators by the macrophage. Although the steps in macrophage cytotoxicity have been well identified, the molecules or recognition structures that macrophages use to bind to tumor cells or to discriminate normal cells from neoplastic cells are unknown. Studies have isolated SV40-transformed tumor cells that were susceptible or resistant to in vitro cytolysis by LPS-activated murine macrophages. The presence of specific RNA tumor virus-induced gp70 was correlated with the resistance to lysis by macrophages. Using Friend leukemia virus (FLV)-transformed cells a different gp70, associated with cells susceptible to macrophage cytotoxicity and not with macrophage resistant FLV-transformed cells, was found. The studies suggest that gp70 may be involved in tumor recognition, but how it is involved is uncertain. Furthermore, involvement of other molecules has not been absolutely disproven. During this research, plans are to investigate the mechanism(s) of macrophage recognition of tumor cells and to biochemically define differences between cells killed or not killed by activated macrophages. (MB)