Else K J, Finkelman F D
School of Biological Sciences, University of Manchester, U.K.
Int J Parasitol. 1998 Aug;28(8):1145-58. doi: 10.1016/s0020-7519(98)00087-3.
Laboratory models of intestinal nematode infection have played an important role in developing our understanding of the immune mechanisms that operate against infectious agents. The type of helper T cell response that develops following infection with intestinal nematode parasites is critical to the outcome of infection. The early events that mediate polarisation of the helper T cell subsets towards either Th1 or Th2 during intestinal nematode infection are not well characterised, but it is likely that multiple factors influence the induction of a Th1 or Th2 type response, just as multiple effector mechanisms are involved in worm expulsion. Costimulatory molecules have been shown to be important in driving T helper cell development down a specific pathway as has the immediate cytokine environment during T cell activation. If helper T cells of the Th2 type gain ascendancy then a protective immune response ensues, mediated by Th2 type cytokines and the effector mechanisms they control. In contrast, if an inappropriate Th1 type response predominates the ability to expel infection is compromised. Equally important is the observation that multiple potential effector mechanisms are stimulated by nematode infection, with a unique combination operating against the parasite depending on nematode species and its life cycle stage. Despite the close association between intestinal nematode infection and the generation of eosinophilia, mastocytosis and IgE it has been difficult to consistently demonstrate a role for these effector cells/molecules in resistance to nematode parasites, although mast cells are clearly important in some cases. It therefore seems that, in general, less classical Th2 controlled effector mechanisms, which remain poorly defined, are probably important in resistance to nematode parasites. Thus, our understanding of both the induction and effector phases remains incomplete and will remain an intense area of interest in the coming years.
肠道线虫感染的实验室模型在增进我们对抵抗感染因子的免疫机制的理解方面发挥了重要作用。感染肠道线虫寄生虫后产生的辅助性T细胞反应类型对感染结果至关重要。在肠道线虫感染期间介导辅助性T细胞亚群向Th1或Th2极化的早期事件尚未得到充分表征，但很可能多种因素影响Th1或Th2型反应的诱导，正如多种效应机制参与蠕虫排出一样。共刺激分子已被证明在驱动T辅助细胞沿着特定途径发育方面很重要，T细胞激活期间的即时细胞因子环境也是如此。如果Th2型辅助性T细胞占优势，那么就会产生由Th2型细胞因子及其控制的效应机制介导的保护性免疫反应。相比之下，如果不适当的Th1型反应占主导，排出感染的能力就会受到损害。同样重要的是，观察到线虫感染会刺激多种潜在的效应机制，根据线虫种类及其生命周期阶段，会有独特的组合作用于寄生虫。尽管肠道线虫感染与嗜酸性粒细胞增多、肥大细胞增多症和IgE的产生密切相关，但很难始终如一地证明这些效应细胞/分子在抵抗线虫寄生虫方面的作用，尽管肥大细胞在某些情况下显然很重要。因此，一般来说，似乎不太经典的、定义仍不明确的Th2控制的效应机制可能在抵抗线虫寄生虫方面很重要。因此，我们对诱导阶段和效应阶段的理解仍然不完整，在未来几年仍将是一个备受关注的领域。
