Ghoneum M, Gill G, Wojdani A, Payne C, Alfred L J
Int J Immunopharmacol. 1987;9(1):71-8. doi: 10.1016/0192-0561(87)90112-3.
C3H mice were injected subcutaneously (s.c.) with a tumorigenic dose (150 micrograms/mouse) of 3-methylcholanthrene (MC), followed by a 24-h injection and subsequent weekly injections of Corynebacterium parvum (CP) i.p. for a total of 100 days. Basal and CP-augmented NK cell activities were measured in controls and treatment groups during pre-tumor and tumor development stages. Basal NK activity in spleen, peripheral blood and lung tissue was enhanced by CP, but was suppressed by MC. A resulting transient MC induced suppression of splenic NK activity at 10 days was partially restored and sustained by CP treatment and immunosuppression was again observed in tumor-bearing compared to control mice. Mice treated with MC alone showed a higher tumor incidence than animals treated with MC + CP at 45-60 days, while there was no difference in tumor incidence in these two treatment groups at 100 days post injection. The mechanism of the observed transient immunosuppression induced by MC appears to be related to an early toxic effect on large granular lymphocytes (LGL) which was decreased at 10 days and again at 100 days in tumor-bearing mice. Although MC did not appear to exert an effect on effector:target cell conjugate formation, an early suppression in the lytic activity of LGL, may have predisposed the animal to malignant transformation of susceptible cells at the site of MC injection.
将致瘤剂量（150微克/只）的3-甲基胆蒽（MC）皮下注射给C3H小鼠，随后进行24小时注射，之后每周腹腔注射微小棒状杆菌（CP），共注射100天。在肿瘤前期和肿瘤发展阶段，对对照组和治疗组的基础NK细胞活性以及CP增强后的NK细胞活性进行了测定。CP增强了脾脏、外周血和肺组织中的基础NK活性，但MC抑制了该活性。MC在第10天导致的脾脏NK活性短暂抑制通过CP治疗得到部分恢复并维持，与对照小鼠相比，荷瘤小鼠再次出现免疫抑制。单独用MC治疗的小鼠在45至60天时的肿瘤发生率高于用MC + CP治疗的动物，而在注射后100天时，这两个治疗组的肿瘤发生率没有差异。观察到的由MC诱导的短暂免疫抑制机制似乎与对大颗粒淋巴细胞（LGL）的早期毒性作用有关，在荷瘤小鼠中，LGL数量在第10天和第100天时均减少。尽管MC似乎对效应细胞：靶细胞结合物的形成没有影响，但LGL裂解活性的早期抑制可能使动物在MC注射部位的易感细胞易于发生恶性转化。
