Molecular negotiations at the host-parasite interface

感染的成败取决于宿主和病原体之间分子对话的结果。对于大型后生动物寄生虫来说尤其如此，例如线虫，它们感染胃肠道和内部组织。宿主抵抗几乎所有寄生虫物种的感染，宿主与寄生虫的相互作用通常是非常特异的。线虫寄生的这一基本方面是如何在分子水平上确定的，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和特异性地调节通常可以防止感染的宿主免疫反应。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。这些相互作用是允许宿主特有的，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，并阐明涉及寄生虫的进化过程。

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.