Infection of Mice Lacking Interleukin-7 (IL-7) Reveals an Unexpected Role for IL-7 in the Development of the Parasite Schistosoma mansoni

A single intradermal administration of recombinant interleukin-7 (IL-7) has been shown to aggravate the course of murine schistosomiasis, to favor the development of Th2-associated antibodies specific for the parasite, and to alter migration kinetics and/or migratory route of the parasite within its vertebrate host. Here we show that after infection of IL-7-deficient mice with Schistosoma mansoni, the predominant parasite-specific humoral response follows a Th1 pattern, and the development of the parasite is greatly impaired. In IL-7-deficient mice, increased numbers of larvae reach the lungs and fewer larvae reach the liver, compared to control mice. In the absence of IL-7, female worms show an altered fecundity, leading to decreased numbers of eggs trapped in the tissues and to an amelioration of the pathology of the infected host. The most striking observation is the blockade of parasite growth in an IL-7-defective environment, leading to dwarf male and female worms. The results of this study have important implications for the role of IL-7 in the host-parasite relationship and show how parasites can disable or evade the host immune response.

已有研究证实，单次皮内注射重组白细胞介素7（recombinant interleukin-7, IL-7）可加重小鼠血吸虫病的病程，促进针对该寄生虫的Th2相关特异性抗体生成，并改变寄生虫在脊椎动物宿主体内的迁移动力学特征及迁移路径。本研究发现，用曼氏血吸虫（Schistosoma mansoni）感染IL-7缺陷小鼠后，宿主主导的寄生虫特异性体液免疫应答呈现Th1型模式，且寄生虫的发育过程受到显著抑制。与对照小鼠相比，IL-7缺陷小鼠体内抵达肺部的幼虫数量增多，而抵达肝脏的幼虫数量减少。在缺乏IL-7的情况下，雌虫的繁殖能力发生异常，导致组织内滞留的虫卵数量减少，并减轻了感染宿主的病理损伤。最引人注目的观测结果是，寄生虫在IL-7缺陷的宿主环境中生长受阻，最终形成矮小的雌雄成虫。本研究结果对于阐明IL-7在宿主-寄生虫相互作用中的调控作用具有重要意义，同时揭示了寄生虫如何规避或拮抗宿主免疫应答。