DEFECTS IN CELL-MEDIATED-IMMUNITY DURING GROWTH OF A SYNGENEIC SIMIAN VIRUS-INDUCED TUMOR
DEFECTS IN CELL-MEDIATED-IMMUNITY DURING GROWTH OF A SYNGENEIC SIMIAN VIRUS-INDUCED TUMOR
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DOI：
10.1002/ijc.2910150118
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发表时间：
1975-01-01
影响因子：
6.4
通讯作者：
LAW, LW
中科院分区：
文献类型：
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作者：
HOWELL, SB;DEAN, JH;LAW, LW
在同基因猴病毒40诱导的肿瘤mKSA生长期间，比较了4种肿瘤特异性细胞介导免疫的试验。通过肿瘤中和试验（Winn试验）、直接肿瘤激发、微量细胞毒性试验和51铬释放淋巴细胞毒性试验检测的免疫力存在重大差异。用Winn试验记录肿瘤的进行性生长，随后免疫力丧失（日食现象）。已经确定，这种日食现象代表了荷瘤宿主的T细胞系统中的病变。这种病变被认为是特定的和无关的解剖肿瘤的位置。在荷瘤动物中，发现产生移植物抗宿主反应的能力和对有丝分裂原的反应能力通常完好无损。在携带晚期肿瘤的小鼠脾脏中发现了能够识别mKSA肿瘤抗原并在手术切除肿瘤后或转移至正常小鼠后重建免疫应答的细胞。没有抑制细胞可以解释日食现象可以证明。在Winn试验中，荷瘤血清不阻断免疫脾细胞的中和活性，免疫细胞即使在荷瘤宿主中也能够中和肿瘤。病变是效应细胞的T细胞前体固有的可能性进行了讨论。
Four assays of tumor‐specific cell‐mediated immunity were compared during growth of a syngeneic Simian‐virus‐40‐induced tumor, mKSA. Major differences were found in immunity detected by the tumor neutralization test (the Winn test), direct tumor challenge, the microcytotoxicity assay and the51chromium‐release lymphocytotoxicity assay. Progressive growth of the neoplasm followed by loss of immunity (the eclipse phenomenon) was documented with the Winn test. It was established that this eclipse phenomenon represented a lesion in the T‐cell system of tumor‐bearing hosts. This lesion was found to be specific and unrelated to anatomic tumor location. The ability to produce graft‐versus‐host reactions, and the ability to respond to mitogens, were found to be generally intact in tumor‐bearing animals. Cells capable of recognizing mKSA tumor antigens and reconstituting an immune response following surgical removal of tumor or upon transfer to normal mice were found in the spleens of mice bearing advanced tumors. No suppressor cells that might account for the eclipse phenomenon could be demonstrated. Tumor‐bearer serum did not block neutralizing activity of immune spleen cells in the Winn test, and immune cells were capable of neutralizing tumor even in tumor‐bearing hosts. The possibility that the lesion is intrinsic to T‐cell precursors of effector cells is discussed.