神经精神性狼疮(NPSLE)是一种难以诊治、致死率高的自身免疫性疾病，致残率和死亡率极高，是目前临床上最棘手的难点之一，其发病机制亟待研究。在NPSLE免疫调控异常中，辅助性T细胞介导B淋巴细胞活化产生多种自身抗体是发病的中心环节。本课题组最近于国内外首次报道泛素羧基端酯酶L1（UCH-L1）及其抗体在发病中的重要生物学意义，为机制研究提供了依据。在后续研究中，本课题将首次对UCH-L1分子的免疫原性进行研究，分别从分子、细胞和动物不同层面，深入研究UCH-L1分子的免疫原性及其抗体在NPSLE中的致病机制，为探索NPSLE的靶向治疗提供分子水平依据。

Neuropsychiatric systemic lupus erythematosus (NPSLE) is one of the most common and complicated autoimmune diseases, with high morbidity and mortality. It is known as the most difficult part in current clinical research. Helper T cell response-mediated activation of B lymphocytes produces a variety of autoantibodies and plays a central role in NPSLE. Our research firstly demonstrated Ubiquitin Carboxyl Hydrolase L1 (UCH-L1) and its antibody have great biologic significance for the pathogenesis of NPSLE, providing evidence for research on the mechanisms of NPSLE. In the next step, the epitope will be identified. The pathogenesis of UCH-L1 and its autoantibody in NPSLE will be explored from aspects of molecule, cell and animal research, which will explore molecular evidence for target therapies.