Ikeda M, Sakagami H, Nishida H, Hatta Y, Fukushima Y
Department of Neurosurgery, Showa University Fujigaoka Hospital, Yokohama, Japan.
Anticancer Res. 1991 Sep-Oct;11(5):1745-9.
Tumor necrosis factor (TNF) dose- and time-dependently stimulated the iodination (incorporation of radioactive iodine into an acid-insoluble fraction) of human peripheral blood polymorphonuclear cells (PMN). The addition of sera obtained from patients with brain tumors, or gastric, pancreatic, hepatocellular, common bile duct or lung carcinoma significantly inhibited TNF-stimulated PMN iodination, whereas sera of normal volunteers were, in general, not inhibitory. TNF-stimulated iodination of human peripheral blood monocytes was almost eliminated by brain tumor patient sera, but was significantly enhanced by normal human sera. Specific [135I] TNF binding to the PMN receptors was significantly increased in the presence of either patient sera or normal sera. These data suggest some mechanism other than modification of TNF receptor binding for expression of the inhibitory action of cancer patient serum.
肿瘤坏死因子（TNF）以剂量和时间依赖性方式刺激人外周血多形核白细胞（PMN）的碘化作用（将放射性碘掺入酸不溶性部分）。添加来自脑肿瘤患者或胃癌、胰腺癌、肝细胞癌、胆总管癌或肺癌患者的血清可显著抑制TNF刺激的PMN碘化作用，而正常志愿者的血清通常无抑制作用。脑肿瘤患者血清几乎消除了TNF刺激的人外周血单核细胞的碘化作用，但正常人血清则显著增强了该作用。在患者血清或正常血清存在的情况下，特异性[135I]TNF与PMN受体的结合显著增加。这些数据表明，癌症患者血清的抑制作用表达存在除TNF受体结合修饰以外的其他机制。
