Rodrick M L, Steele G, Ross D S, Lahey S J, Deasy J M, Rayner A A, Harte P J, Wilson R E, Munroe A E, King V P
J Natl Cancer Inst. 1983 Jun;70(6):1113-8.
Inbred male WF rats were given im injections of one of two antigenically and histologically distinct syngeneic tumor isografts, adenocarcinoma DMH-W 163 or spontaneous renal cell carcinoma SPK. Serum and peripheral blood lymphocytes were harvested from tumor-bearing and normal age-matched controls before and after isograft challenge at weekly intervals. Serial circulating immune complex (CIC) levels were quantitated by polyethylene glycol (PEG) insolubilization. T-cell mitogen responses to phytohemagglutinin (PHA) and concanavalin A (Con A) were followed serially. Tumor growth was measured at least weekly. PEG-CIC values rose early after tumor injection, increased with tumor growth, and declined in some animals just before death. Mitogen response to PHA was significantly decreased in isografted tumor-bearing rats, particularly at later stages of tumor development, compared to normal uninoculated controls. Responses to Con A were variable, and suppression was not always seen in tumor bearers. In animals that did not have progressive tumor growth after isograft injection, PEG-CIC levels did not change and responses to PHA were not suppressed. Patterns of CIC change and responses to PHA were not affected by differences in tumor histology or growth rates. Thus serial CIC levels measured by the PEG assay correlate with tumor growth and precede nonspecific suppression of T-cell mitogenic response in these animal tumor models.
近交系雄性WF大鼠接受皮下注射两种抗原性和组织学上不同的同基因肿瘤移植瘤之一,即腺癌DMH-W 163或自发性肾细胞癌SPK。在同基因移植瘤攻击前后,每周从荷瘤大鼠和年龄匹配的正常对照大鼠中采集血清和外周血淋巴细胞。通过聚乙二醇(PEG)沉淀法对循环免疫复合物(CIC)水平进行连续定量。连续监测T细胞对植物血凝素(PHA)和刀豆蛋白A(Con A)的丝裂原反应。至少每周测量一次肿瘤生长情况。PEG-CIC值在肿瘤注射后早期升高,随肿瘤生长而增加,在一些动物濒死时下降。与未接种的正常对照相比,荷同基因移植瘤大鼠对PHA的丝裂原反应显著降低,尤其是在肿瘤发展的后期。对Con A的反应各不相同,肿瘤荷瘤动物并不总是出现抑制现象。在同基因移植瘤注射后肿瘤无进展生长的动物中,PEG-CIC水平没有变化,对PHA的反应也未受到抑制。CIC变化模式和对PHA的反应不受肿瘤组织学或生长速率差异的影响。因此,在这些动物肿瘤模型中,通过PEG法测定的连续CIC水平与肿瘤生长相关,并先于T细胞丝裂原反应的非特异性抑制。