Infection of mice lacking interleukin-7 (IL-7) reveals an unexpected role for IL-7 in the development of the parasite Schistosoma mansoni

Infection of mice lacking interleukin-7 (IL-7) reveals an unexpected role for IL-7 in the development of the parasite Schistosoma mansoni
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DOI:
10.1128/iai.67.8.4183-4190.1999
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发表时间:
1999-08-01
影响因子:
3.1
通讯作者:
Auriault, C
Auriault, C
中科院分区:
医学2区
文献类型:
--
作者:
Wolowczuk, I;Nutten, S;Auriault, C

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重组白细胞介素-7 (IL-7)单次皮内给药已被证明可加重小鼠血吸虫病的病程,有利于寄生虫特异性th2相关抗体的产生,并改变寄生虫在其脊椎动物宿主内的迁移动力学和/或迁移途径。本研究表明,在感染了il -7缺陷小鼠后,主要的寄生虫特异性体液反应遵循Th1模式,并且寄生虫的发育受到极大损害。在缺乏il -7的小鼠中,与对照组小鼠相比,到达肺部的幼虫数量增加,到达肝脏的幼虫数量减少。在缺乏IL-7的情况下,雌性蠕虫表现出繁殖能力的改变,导致组织中捕获的卵数量减少,并改善受感染宿主的病理。最引人注目的观察结果是,在il -7缺陷的环境中,寄生虫的生长被阻断,导致雄性和雌性蠕虫变得矮小。本研究结果对IL-7在宿主-寄生虫关系中的作用具有重要意义,并揭示了寄生虫如何使宿主免疫反应失效或逃避。
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.