Coulson P S, Wilson R A
Department of Biology, The University of York, United Kingdom.
Infect Immun. 1997 Jan;65(1):42-8. doi: 10.1128/iai.65.1.42-48.1997.
The effector mechanism, which operates against challenge parasites in the lungs of C57BL/6 mice vaccinated once with irradiated cercariae of Schistosoma mansoni, is mediated by CD4+ T helper lymphocytes. However, adoptive transfer of immunity from vaccinated donors to naive recipients by using sensitized T cells has not proved successful. One explanation may be that the recruitment of sensitized T lymphocytes to the lungs by vaccinating parasites to arm that organ is not reproduced by transfer protocols. We have used the technique of parabiosis, as a means of adoptive transfer, to demonstrate the relevance of pulmonary T cells to protection. Sensitized and naive partners were joined surgically for a 28-day period, coincident with priming of the immune system. A vascular union rapidly developed, and sensitized T cells were detected in the spleens of the naive partners. When parabionts were challenged percutaneously 10 days after separation, the level of immunity transferred to the naive partners was approximately two-thirds that of their vaccinated counterparts. The naive partners, unlike the vaccinated animals, did not recruit lymphocytes to the lungs during the priming period. In contrast, after percutaneous challenge, schistosome-specific lymphocytes were recruited to the lungs of both separated parabionts. The importance of lymphocytes recruited to the lungs during the primary response was revealed by an intravenous challenge with lung schistosomula; this eliminates the opportunity for secondary immune responses prior to parasite arrival in the lungs. In this situation, the vaccinated partners showed 47% immunity while the naive partners were not protected. We conclude that the presence of specific T cells in the lungs at the time of challenge confers a significant advantage, permitting a more effective recall response than in animals lacking such resident cells.
在经曼氏血吸虫辐照尾蚴单次免疫的C57BL/6小鼠肺部，针对感染寄生虫发挥作用的效应机制由CD4 +辅助性T淋巴细胞介导。然而，通过使用致敏T细胞将免疫从已免疫供体过继转移至未致敏受体的方法尚未成功。一种解释可能是，通过接种寄生虫使致敏T淋巴细胞募集至肺部从而武装该器官的过程，无法通过转移方案重现。我们采用联体共生技术作为过继转移的一种手段，来证明肺部T细胞与保护作用的相关性。将致敏和未致敏的小鼠通过手术连接28天，这与免疫系统的启动时间一致。血管连接迅速形成，在未致敏小鼠的脾脏中检测到了致敏T细胞。联体小鼠在分离后10天经皮感染，转移至未致敏小鼠的免疫水平约为其已免疫对应小鼠的三分之二。与已免疫动物不同，未致敏小鼠在启动期未向肺部募集淋巴细胞。相反，经皮感染后，血吸虫特异性淋巴细胞被募集至两只分离的联体小鼠的肺部。用肺期血吸虫童虫进行静脉感染揭示了初次应答期间募集至肺部的淋巴细胞的重要性；这消除了寄生虫到达肺部之前发生二次免疫应答的机会。在这种情况下，已免疫小鼠显示出47%的免疫力，而未致敏小鼠未受到保护。我们得出结论，感染时肺部存在特异性T细胞具有显著优势，与缺乏此类驻留细胞的动物相比，能产生更有效的回忆应答。
