Yang C, Nowotny A
Infect Immun. 1974 Jan;9(1):95-100. doi: 10.1128/iai.9.1.95-100.1974.
As reported earlier, an intraperitoneal injection of 1 mug of endotoxin (ET) from Serratia marcescens rendered mice resistant against the nonspecific mouse ascites tumor TA3-Ha upon challenge 24 h after pretreatment with ET. Further studies were aimed at the elaboration of conditions which achieved maximal resistance. It appears that (i) a 10-mug dose of ET was approximately the optimal dose for protection; (ii) pretreatment with ET 3 to 0 days prior to tumor challenge gave best protection; and (iii) the intravenous injection of ET showed a lower protection against the tumor than intraperitoneal application. Studies on the mechanism of ET protection indicate that (i) ET does not have a direct cytotoxic effect on tumor cells; (ii) normal spleen cells exposed to ET in vitro can adoptively transfer protection against tumor; and (iii) spleen cells activated in vivo by intravenous injection of ET can adoptively transfer protection. The possible involvement of mononuclear cells is discussed.
如先前报道,腹腔注射1微克粘质沙雷氏菌的内毒素(ET)可使小鼠在经ET预处理24小时后受到攻击时,对非特异性小鼠腹水瘤TA3-Ha产生抗性。进一步的研究旨在阐明实现最大抗性的条件。似乎(i)10微克剂量的ET大约是保护的最佳剂量;(ii)在肿瘤攻击前3至0天用ET预处理可提供最佳保护;(iii)静脉注射ET对肿瘤的保护作用低于腹腔注射。关于ET保护机制的研究表明,(i)ET对肿瘤细胞没有直接的细胞毒性作用;(ii)体外暴露于ET的正常脾细胞可过继性转移对肿瘤的保护作用;(iii)通过静脉注射ET在体内激活的脾细胞可过继性转移保护作用。文中讨论了单核细胞可能的参与情况。