Molecular negotiations at the host-parasite interface

感染的成功或失败取决于宿主和病原体之间分子对话的结果。对于大型后生寄生虫，如线虫，尤其如此，它们会感染胃肠道和内部组织。宿主可以抵抗几乎所有寄生虫的感染，而且宿主与寄生虫的相互作用通常是非常特异性的。线虫寄生的这个基本方面是如何在分子水平上决定的仍然是一个谜。我们的驱动假设是，寄生线虫分泌的分子选择性地和特异性地调节宿主的免疫反应，通常会防止感染。寄生虫分子在受体水平和基因调控水平上与宿主免疫细胞相互作用。这些相互作用对容许宿主是特异性的，并建立了宿主-寄生虫特异性的分子基础。了解寄生虫用来完成这种免疫调节的分子将揭示宿主-寄生虫特异性的分子基础，并阐明寄生的进化过程。

The success or failure of an infection depends on the outcome of a molecular dialog between host and pathogen. This is especially true for large metazoan parasites such as nematodes, which infect the gastrointestinal tract and internal tissues. Hosts resist infection by almost all parasite species, and host-parasite interactions are typically quite specific. How this fundamental aspect of nematode parasitism is determined at the molecular level remains a mystery. Our driving hypothesis is that molecules secreted by parasitic nematodes selectively and specifically modulate host immune responses that would normally prevent infection. Parasite molecules interact with host immune cells at the receptor level and at the level of gene regulation. These interactions are specific for permissive hosts and establish the molecular basis of host-parasite specificity. Understanding the molecules used by parasites to accomplish this immunomodulation will reveal the molecular basis for host-parasite specificity and illuminate the evolutionary processes involved in parasitism.