目前在我国造成终末期肾衰竭即尿毒症的第一位病因是肾小球疾病，免疫炎症机制是此类疾病发生发展的核心所在。本群体将在现有工作的基础上，进一步探索肾小球肾炎的免疫炎症发病机制，包括：利用抗原决定簇研究揭示自身免疫性肾小球肾炎的病因学；阐明自身免疫性肾小球肾炎的补体异常活化及其调控机制，发现新的治疗靶点；阐明糖基化缺陷的IgA1及其抗体在IgA肾病发病机制中的作用。通过这些研究，不但可进一步阐明肾小球肾炎的病因和发病机制，同时有望发现新的治疗靶点。

Up to now, the leading cause of end-stage renal disease in China is still glomerular nephritis. Immune and inflammation mechanism play a key role in the pathogenesis and progression of the disease. Based on our previous work, we will further explore the immune and inflammation pathogenesis of glomerular nephritis, including: critical T cell epitope of autoimmune glomerulonephritis and possible etiology through molecular mimicry theory; abnormal complement activation and its regulation mechanism in autoimmune glomerulonephritis; specific types of aberrant glycosylated IgA1 and their antibodies in the pathogenesis of IgA nephropathy. By means of these investigations, we will try to elucidate the pathogenesis and progress of glomerular nephritis and to provide evidence for developing novel therapeutic targets for the disease.