Pattern recognition receptors and the recruitment and differentiation of myeloid cells in inflammation.

该研究的主要目的是了解免疫受体dectin-1如何控制真菌感染后的炎症反应，并开发新的实验小鼠模型，以促进这些和相关的炎症研究。在感染时，身体启动炎症反应，其目的是招募专门的免疫细胞到感染部位并遏制感染性生物体。这些细胞在其表面表达受体，这些受体能够识别微生物的不同成分。许多细胞表面受体对多种微生物成分的集体识别使免疫细胞能够“识别”感染的生物体并促进适当的免疫应答的发展。Dectin-1是参与识别真菌的关键受体，其结合真菌特异性碳水化合物（β-葡聚糖）。我们已经证明，这种受体是小鼠真菌感染后正常炎症反应所必需的，它的缺乏导致对感染的易感性增加。真菌感染是重要的，因为它们的频率增加，作为现代医学和免疫系统中获得性缺陷的结果。这些研究将帮助我们了解正常的保护性免疫反应是如何发生的真菌感染。

The main aims of the research are to understand how the immune receptor dectin-1 controls the inflammatory response after fungal infection and to develop new experimental mouse models to facilitate these and related studies of inflammation.At the time of an infection, the body initiates an inflammatory response, the aim of which is to recruit specialised immune cells to the site of infection and contain the infectious organism. The cells express receptors on their surface that are able to recognise distinct components of microorganisms. The collective recognition of multiple microbial components by many cell surface receptors enables the immune cells to ‘identify‘ the infecting organism and promote the development of an appropriate immune response.Dectin-1 is a key receptor involved in the recognition of fungi that binds to fungal specific carbohydrates (beta-glucans). We have shown that this receptor is essential for a normal inflammatory response after fungal infection of mice and that its absence results in increased susceptibility to infection.Fungal infections are important because of their increasing frequency as a consequence of modern medicine and acquired defects in the immune system. These studies will help us understand how a normal protective immune response to fungal infection occurs.