申请人致力于探究NOD样受体的活化机制、调控网络及疾病相关性。主要研究成果有：1）发现NLRP3炎症小体活化在2型糖尿病(T2D)发生中的关键致病作用，提示NLRP3炎症小体是潜在的T2D干预靶点 (Nat Immunol, 2010)。2）发现线粒体损伤在NLRP3 炎症小体活化中的关键作用，并证明RNA病毒通过RIP1-RIP3-DRP1信号通路诱导线粒体损伤和炎症小体活化 (Nature, 2011; Nat Immunol, 2014)。3）发现外源性物质Omega-3脂肪酸及内源性物质多巴胺均可通过抑制NLRP3炎症小体缓解炎症性疾病，并阐明其机制(Immunity, 2013; Cell, 2015)。4）发现NOD2可通过识别肠道共生菌维持肠道上皮内淋巴细胞稳态并抑制肠炎发生(J Exp Med, 2013)。论文他引1500余次，其中4项工作被F1000收录和推荐。

The applicant focused on studying the activation, regulation and disease relevance of NOD-like receptors (NLRs). The major achievements include: 1) we found the important role of NLRP3 inflammasome in the development of type 2 diabetes (T2D), suggesting NLRP3 inflammaosme as a potential target for treatment of T2D; 2) we clarified the critical role of mitochondrial damage and ROS production in NLRP3 inflammasome actiavtion and found that RNA viruses could promote mitochondrial damage and NLRP3 inflammasome activation via RIP1-RIP3-DRP1 signaling pathway; 3) we found that exogenous omega-3 fatty acids or endogenous dopamine could inhibit NLRP3 inflammasome activation and prevent NLRP3-drivern inflammatory diseases; 4) we found that NOD2 signaling could maintain the homeostasis of intestinal intraepithelial lymphocytes (IELs) via recognition of microbiota and prevent the development of colitis. These results have been published on some top journals as first-author or corresponding author, including Nature, Nat Immunol, Cell, Immunity and J Exp Med. These papers have been cited over 1500 times by SCI-recruited journals, including Annual Rev Immunol、Nature、Science et al. Four of them have been recommended by "Faculty 1000".