ANTI-TUMOR IMMUNITY IN LYMPHOCYTE-B-DEPRIVED MICE .3. IMMUNITY TO PRIMARY MOLONEY SARCOMA VIRUS-INDUCED TUMORS

ANTI-TUMOR IMMUNITY IN LYMPHOCYTE-B-DEPRIVED MICE .3. IMMUNITY TO PRIMARY MOLONEY SARCOMA VIRUS-INDUCED TUMORS
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DOI:
10.1002/ijc.2910290320
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发表时间:
1982-01-01
影响因子:
6.4
通讯作者:
FELDMAN, M
FELDMAN, M
中科院分区:
医学1区
文献类型:
--
作者:
GORDON, J;HOLDEN, HT;FELDMAN, M

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在B淋巴细胞功能被抗IgM抗体长期抑制的小鼠中注射莫洛尼肉瘤病毒(MSV)后,研究了肿瘤诱导和对肿瘤的免疫。使用了两种MSV制剂:一种在正常成年小鼠中产生均匀消退的肿瘤,另一种在大多数接受者中产生逐渐生长的肿瘤。肿瘤发生率、平均肿瘤大小和消退克里思均未通过抗IgM治疗改变。而由回归病毒诱导的肿瘤在19只NRG[正常兔球蛋白]治疗和29只未治疗的受体中均被排斥,在23只B淋巴细胞剥夺小鼠中有2只获得了持续生长。在来自该组的另外9只小鼠中,明显排斥之后是在初始肿瘤部位的肿瘤复发。持续的生长伴随着广泛的转移。这些肿瘤可自由移植到正常同基因受体。在给予进展病毒的24只抗IgM治疗小鼠中的7只中也检测到转移和可移植性,但在对照动物中未观察到。尽管脾脏中存在高水平的特异性细胞毒性T淋巴细胞,但仍获得复发和转移。B淋巴细胞或其产物在宿主对MSV诱导的肿瘤的保护中起重要作用。
Tumor induction and immunity to tumors were studied following the injection of Moloney sarcoma virus (MSV) into mice in which B-lymphocyte functions had been suppressed by the chronic administration of anti-IgM antibodies. Two preparations of MSV were used: one gives rise to tumors which uniformly regress in normal adult mice, and another elicits progressively growing tumors in the majority of recipients. The tumor incidence, mean tumor size and tempo of regression were not modified by treatment with anti-IgM. Whereas tumors induced by the regressor virus were all rejected in 19 NRG[normal rabbit globulin]-treated and 29 untreated recipients, continued growth was obtained in 2 of 23 B-lymphocyte-deprived mice. In 9 additional mice from this group, apparent rejection was followed by tumor recurrence at the site of the initial tumor. Continued growth was accompanied by widespread metastasis. These tumors were freely transplantable to normal syngeneic recipients. Metastasis and transplantability were also detected in 7 of 24 anti-IgM-treated mice given progressor virus but were not seen in the control animals. Recurrence and metastasis were obtained despite the presence of high levels of specific cytotoxic T lymphocytes in the spleen. B lymphocytes or their products play an essential role in host protection against MSV-induced tumors.