特邀学术报告
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时间：2017年1月9日9点30分
地点：资环楼105 室（芭田报告厅）
主 持 人：刘定祥 教授
报 告 人：郑 杰 博士 美国斯克利普斯研究所，分子医学部
报告题目：Dysregulated checkpoints compromise immune tolerance of self-RNA during RIG-I mediated autoimmunity
报告人简介：
郑杰博士，本科就读于中国药科大学，2015年博士毕业于新加坡南洋理工大学，随后在美国斯克利普斯研究所分子医学部进行博士后工作至今。其研究领域为利用蛋白质谱分析手段研究免疫系统关键蛋白的结构与功能，发表论文数十篇，主要成果发表于Frontiers in microbiology、 Nature Communications、Nucleic acids research等国际知名期刊。
报告简介：
The cytosolic innate immunity receptor Retinoic Acid Inducible Gene-I (RIG-I) recognizes viral 5’-triphosphorylated RNA (5’ppp) for immune surveillance against viral infection. However, dysregulated RIG-I proofreading evades immune tolerance of endogenous RNAs leading to autoimmune disease. Yet the precise mechanism of such dysregulation remains unknown. Herein, by using hydrogen/deuterium exchange mass spectrometry, we show that immune tolerance and stimulation of self-RNAs and viral RNAs are achieved through multiple checkpoints during RIG-I proofreading. In contrast, unrestrained RNA surveillance and dysregulated checkpoints coordinated by disordered RIG-I proofreading could occur through distinct mechanisms during different stages of RIG-I signaling relay that cumulatively result in a nano-mechanical transition of the receptor to a signaling competent state. And this principle may be applicable to MDA5 as well as other innate immunity receptor mediated autoimmune diseases. Confirmation of these mechanisms will potentially assist therapies for treatment of autoimmunity that drive immune defense against viral infections while minimizing autoimmune disorders.
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