The role of C-type lectin receptors in adaptive anti-fungal immunity

真菌感染对人类健康造成巨大负担，特别是对免疫系统改变的个体。如果我们要利用这些知识来开发对抗这些感染的新疗法，对免疫系统如何提供对真菌疾病的保护有更深入的了解是至关重要的。我们之前发现，在免疫细胞表面表达的一种关键分子，称为Dectin-1，在抗真菌免疫中起着核心作用。我们随后的研究表明，Dectin-1保护胃肠道免受白色念珠菌感染，白色念珠菌是一种真菌生物，通常与人类有关，但在免疫功能受损的个体中可能导致毁灭性的疾病。值得注意的是，我们发现Dectin-1的缺失导致白色念珠菌感染后的异常免疫反应，导致感染胃肠道中重要功能细胞（称为t细胞）的损失。我们最近确定Dectin-1控制着一组新分子的表达，这些分子参与了这些关键t细胞反应的发展。在这个应用中，我们建议表征这些令人兴奋的新分子的表达和功能，并确定它们如何在胃肠道中促进抗真菌免疫。

Fungal infections pose an enormous burden on human health, particularly in individuals with altered immune systems. Developing a greater understanding of how the immune system actually provides protection against fungal diseases is critical if we are to use this knowledge to develop novel therapies to combat these infections. We previously discovered that a key molecule expressed on the surface of immune cells, called Dectin-1, plays a central role in antifungal immunity. Our subsequent research revealed that Dectin-1 protects the gastrointestinal (GI) tract from infection with Candida albicans, a fungal organism that is commonly associated with humans, but that can cause devastating diseases in individuals whose immune functions are compromised. Notably, we found that absence of Dectin-1 led to aberrant immune responses following infection with C. albicans, which resulted in a loss of important functional cells, called T-cells, in the infected GI tract. We have recently determined that Dectin-1 controls expression of a novel group of molecules that are involved in the development of these critical T-cell responses. In this application, we propose to characterise the expression and function of these exciting new molecules and establish how they contribute to antifungal immunity in the GI tract.