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2018.10.31 苏立山教授(美国北卡罗来纳大学)学术报告

时间:2018年10月25日 访问次数:434

报告题目:How does HIV-1 cause AIDS? 
                  Novel Mechanisms and Therapeutic Targets of Human Inflammatory Diseases
报告人苏立山  教授 
主持人:冯新华  教授
时   间:2018年10月31日(周三)下午4点
地   点:纳米楼457报告厅

报告人简介:

        苏立山教授于1982年获山东大学生物系微生物学学士学位,1989年获哈佛大学病毒学博士学位,随后在斯坦福大学从事免疫学和造血干细胞方向的博士后研究。1993年至1996年在SyStemix /Sandoz (Novartis/诺华)公司担任高级研究员,研究HIV致病机制和艾滋病的基因治疗。1996年加入美国北卡罗来纳大学,现任微生物学和免疫学系教授,莱恩伯格综合癌症中心和UNC传染病中心成员。

       苏立山教授在加入美国北卡罗来纳大学后,其实验室通过人源化小鼠模型鉴定了多个HIV-1发病的病毒学和免疫学新机制。同时,苏教授的实验室建立了免疫系统和肝脏细胞的人源化小鼠,用于探索乙型、丙型肝炎感染过程中免疫应答和肝纤维化的研究。

讲座摘要:

Plasmacytoid dendritic cells (pDC) are the major type I interferon (IFN-I) producing cells and play important roles in antiviral immune responses during acute virus infection. We have recently functionally defined the HIV-pDC-IFN axis in HIV-1 immunopathogenesis, and studied the mechanisms of pDC/IFN-induced immune suppression, and its role in HIV reservoir persistence. We have discovered that blocking the pDC/INF-I axis during HIV infection reverses all HIV-related diseases even in the presence of higher levels of HIV replication. We further show that low levels of pDC/IFN-I signaling contribute to the immune dysfunction and foster HIV-1 persistence in cART-treated hosts. During suppressive HIV/ART,transient depletion of pDC or blocking IFNAR, or its downstream mediators,has been shown to provide a novel strategy to enhance immune recovery and to control HIV-1 reservoirs.Our findings not only functionally reveal the pDC/IFN-I axis in HIV-1 and other inflammatory diseases, the IFNAR blocking and pDC-depleting mAb will also be developed into novel therapeutics to enhance immune recovery to treat HIV-associated diseases and cancers.