Université de Perpignan Via Domitia, Perpignan F-66860, France.
Dev Comp Immunol. 2012 May;37(1):1-8. doi: 10.1016/j.dci.2011.09.002. Epub 2011 Sep 16.
Coevolutionary dynamics in host-parasite interactions potentially lead to an arms race that results in compatibility polymorphism. The mechanisms underlying compatibility have remained largely unknown in the interactions between the snail Biomphalaria glabrata and Schistosoma mansoni, one of the agents of human schistosomiasis. This review presents a combination of data obtained from field and laboratory studies arguing in favor of a matching phenotype model to explain compatibility polymorphism. Investigations focused on the molecular determinants of compatibility have revealed two repertoires of polymorphic and/or diversified molecules that have been shown to interact: the parasite antigens S. mansoni polymorphic mucins and the B. glabrata fibrinogen-related proteins immune receptors. We hypothesize their interactions define the compatible/incompatible status of a specific snail/schistosome combination. This line of thought suggests concrete approaches amenable to testing in field-oriented studies attempting to control schistosomiasis by disrupting schistosome-snail compatibility.
宿主-寄生虫相互作用中的协同进化动态可能导致军备竞赛,从而导致相容性多态性。在蜗牛 B. glabrata 和曼氏血吸虫之间的相互作用中,后者是人类血吸虫病的病原体之一,相容性的机制在很大程度上仍然未知。本综述结合了从现场和实验室研究中获得的数据,提出了一个匹配表型模型来解释相容性多态性。对相容性分子决定因素的研究揭示了两个多态性和/或多样化的分子库,这些分子已被证明可以相互作用:寄生虫抗原 S. mansoni 多态粘蛋白和 B. glabrata 纤维蛋白原相关蛋白免疫受体。我们假设它们的相互作用定义了特定蜗牛/血吸虫组合的相容/不相容状态。这种思路提出了具体的方法,适用于以现场为导向的研究,试图通过破坏血吸虫-蜗牛的相容性来控制血吸虫病。