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小鼠在氨基甲酸乙酯和N-亚硝基甲基脲致白血病过程中的免疫抑制

Immunodepression during urethane and N-nitrosomethylurea leukaemogenesis in mice.

作者信息

Parmiani G, Colnaghi M I, Della Porta G

出版信息

Br J Cancer. 1971 Jun;25(2):354-64. doi: 10.1038/bjc.1971.46.

Abstract

Five injections of urethane, 1 mg./g. body weight to suckling mice markedly reduced the primary immune response against sheep red blood cells assessed by splenic plaque forming cells (PFC) determination and haemagglutinin (HA) titration. The immunological impairment lasted for about 50 days after the end of the treatment. The secondary response tested by HA titration was not affected. A lower dose of urethane (0.5 mg./g.) produced only a delay of the primary HA response. A single neonatal dose of N-nitrosomethylurea (NMU) caused a profound immunodepression evaluated as HA titre and number of PFC. Both primary and secondary responses were still depressed when tested at 50 and 90 days of age respectively. No clear correlation between the degree of immunodepression and lymphoma development was found.

摘要

给乳鼠注射五次氨基甲酸乙酯,剂量为1毫克/克体重,通过脾集落形成细胞(PFC)测定和血凝素(HA)滴定评估,可显著降低其对绵羊红细胞的初次免疫反应。治疗结束后,免疫损伤持续约50天。通过HA滴定检测的二次反应未受影响。较低剂量的氨基甲酸乙酯(0.5毫克/克)仅使初次HA反应延迟。单次新生期剂量的N-亚硝基甲脲(NMU)导致以HA滴度和PFC数量评估的严重免疫抑制。分别在50日龄和90日龄进行检测时,初次和二次反应均仍受抑制。未发现免疫抑制程度与淋巴瘤发生之间有明显相关性。

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