Aitken R, Coulson P S, Dixon B, Wilson R A
Department of Biology, University of York, Heslington, England.
Am J Trop Med Hyg. 1987 Nov;37(3):570-7. doi: 10.4269/ajtmh.1987.37.570.
Vaccination of mice with attenuated cercariae of Schistosoma mansoni induces specific acquired resistance to challenge infection. This resistance is immunologically-mediated, possibly via a delayed-type hypersensitivity. Studies of parasite migration have shown that the protective mechanism operates most effectively in the lungs of vaccinated mice. We have probed the mechanism by exposing mice to 500 rads of gamma radiation before challenge infection. Our results show that the effector mechanism operative against challenge larvae is resistant to radiation. In contrast, classical immune responses are markedly suppressed by the same treatment. While leukocyte populations in the blood fall dramatically after irradiation, numbers of cells recoverable by bronchoalveolar lavage are unaffected. We suggest that vaccination with attenuated cercariae establishes populations of sensitized cells in the lungs which trigger the mechanism of resistance when challenge schistosomula migrate through pulmonary capillary beds. Although the cells may be partially disabled by irradiation, they remain responsive to worm antigens and thereby capable of initiating the elimination mechanism. This hypothesis would explain the radiation resistance of vaccine-induced immunity to S. mansoni.
用曼氏血吸虫减毒尾蚴对小鼠进行疫苗接种可诱导对攻击感染的特异性获得性抵抗力。这种抵抗力是由免疫介导的，可能通过迟发型超敏反应。对寄生虫迁移的研究表明，保护机制在接种疫苗的小鼠肺部最为有效。我们通过在攻击感染前让小鼠暴露于500拉德的γ辐射来探究其机制。我们的结果表明，针对攻击幼虫起作用的效应机制对辐射具有抗性。相比之下，经典免疫反应会受到相同处理的显著抑制。虽然照射后血液中的白细胞数量急剧下降，但通过支气管肺泡灌洗可回收的细胞数量不受影响。我们认为，用减毒尾蚴进行疫苗接种会在肺部建立致敏细胞群体，当攻击血吸虫幼虫迁移通过肺毛细血管床时，这些细胞会触发抗性机制。尽管这些细胞可能会因辐射而部分失能，但它们仍对蠕虫抗原产生反应，从而能够启动清除机制。这一假设可以解释疫苗诱导的对曼氏血吸虫免疫力的辐射抗性。
