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体内经5-(3,3-二甲基-1-三氮烯基)咪唑-4-甲酰胺(DIC)处理的淋巴瘤细胞的细胞动力学和免疫原性

Cell kinetics and immunoegenicity of lymphoma cells treated with 5-(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (DIC) in vivo.

作者信息

Silvestrini R, Testorelli C, Goldin A, Nicolin A

出版信息

Int J Cancer. 1977 May 15;19(5):664-9. doi: 10.1002/ijc.2910190510.

Abstract

A cycle of treatment with antineoplastic compounds may alter the immunologic properties of experimental tumors leading to an increased survival of syngeneic hosts as compared to that observed with the original parental tumors. However, a loss of growth potential in drug-treated tumors might account for this preferential rejection by syngeneic or by allogeneic animals. In the present study the cell cycle kinetics of parental (L1210 and L5178Y) and DIC-altered leukemic cells (L1210/DIC; L5178Y/DIC) has been evaluated by the establishment of labelled mitosis curves. The in vitro DNA synthesis and cell loss were also investigated. The experimental results indicate that no significant differences in the above properties were present for parental and corresponding drug-treated leukemic sublines. Immuno-depressed allogeneic mice were more resistant to lymphoma challenge when inoculated with the DIC-sublines than with the parental lines. On adoptive transfer of immune lymphocytes there was increased survival of allogeneic animals challenged with DIC cells, attributable to an additional immune response to DIC-induced antigens. Thus, parental or DIC-tumors showed similar tumorigenic characteristics, and the increased allogeneic host survival to DIC-cell challenge may be attributed to an additional immune response of the animal DIC-induced antigens.

摘要

用抗肿瘤化合物进行的一个治疗周期可能会改变实验性肿瘤的免疫特性,导致同基因宿主的生存期比用原始亲本肿瘤观察到的生存期有所延长。然而,药物处理过的肿瘤生长潜能的丧失可能是同基因或异基因动物出现这种优先排斥现象的原因。在本研究中,通过建立标记有丝分裂曲线,评估了亲本(L1210和L5178Y)及经二氯二乙胺(DIC)改变的白血病细胞(L1210/DIC;L5178Y/DIC)的细胞周期动力学。还研究了体外DNA合成和细胞丢失情况。实验结果表明,亲本白血病细胞系和相应的药物处理过的白血病亚系在上述特性方面没有显著差异。免疫抑制的异基因小鼠接种DIC亚系时比接种亲本系时对淋巴瘤攻击更具抵抗力。在免疫淋巴细胞的过继转移中,用DIC细胞攻击的异基因动物的生存期延长,这归因于对DIC诱导抗原的额外免疫反应。因此,亲本肿瘤或DIC处理的肿瘤表现出相似的致瘤特性,而异基因宿主对DIC细胞攻击的生存期延长可能归因于动物对DIC诱导抗原的额外免疫反应。

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