白念珠菌属于人体正常菌群，同时也是一种重要的机会致病菌，能够引起致命性的侵袭性感染。Card9是宿主抗真菌免疫的重要调控因子。目前已证实Card9与细胞膜表面模式识别受体CLRs形成的Card9/CLRs通路是抗白念珠菌免疫的一条极为重要的通路，是宿主免疫的第一道防线。而当白念珠菌侵入细胞后，NLRP3炎症小体作为重要的胞内模式识别受体，构成固有免疫的第二道防线。目前Card9通过调控其他模式识别受体在抗白念珠菌感染中的研究较少，但有研究发现Card9在抗某些微生物免疫中可能对NLRP3炎症小体具有负调控作用。我们设想Card9可能通过对不同信号通路的正调控或负调控作用，维持了抗病原体免疫与宿主炎症反应的平衡，以达到更好的抗病原体免疫效果。我们期望通过阐明Card9蛋白对于NLRP3炎症小体通路的具体调节作用及机制，来证实我们的设想，为更好地理解宿主抗白念珠菌免疫奠定基础。

Candida albicans is a common commercial fungi as well as an opportunistic pathogen which could causing life-threatening infections. Card9 is a key regulator in the host immune against fungi. It has been proved that Card9/CLRs pathway is a significant pathway serving as the first defense against Candida albicans. While Candida albicans invades inside the host cells, NLRP3 inflammasome serves as the second defense as an intracellular pattern recognition receptor. There are very few reports of the regulation of other pattern recognition receptors by Card9 in the host defense against Candida albicans. However, Card9 may be a negative regulator in host defense against certain pathogen. We postulate that Card9 may play different roles in signaling pathways under different pattern recognition receptor, and maintain a steady state between host immune against Candida albicans and inflammation to achieve better effects of host immune against Candida albicans. We aim to prove the roles of Card9 in the regulation of NLRP3 inflammasome for a better understanding of the host immune against Candida albicans.