Macrophages and T lymphocytes are major immune cells which mediate inflammatory responses and Immune-mediated Inflammatory Diseases, including autoimmune diseases, infection, and inflammation-related cancer. We are interested in identify key kinases, enzymes or signaling molecules in macrophages and T cells that mediate cell migration, inflammation and immune surveillance. Especially we are interested in how lipid/cholesterol metabolism regulates function of macrophage, CD8+ T cell and MDSC (Myeloid-derived suppressor cells) during anti-viral and anti-tumor responses. As the corresponding author, I have published 20 SCI papers, including IMMUNTIY, NAT MICROBIOL, JCI, JEM, EMBO MM, CELL RES. I obtained several awards, including “National Science Fund for Distinguished Young Scholars” and “Outstanding Graduate Student Instructor, Chinese Academy of Sciences”.
The title of my talk: The function and mechanism of macrophages against infection
Although TLR4 triggers NF-κB activation to produce proinflammatory cytokines for bacteria clearance, excessive activation of the TLR4 signalling pathway could lead to serious inflammatory diseases, including septic shock and inflammation-related tumour. Septic shock causes high death rate reaching 35-85%, and the proinflammatory cytokines could promote tumour development. We also investigate the underline mechanism of how macrophages regulate IFN production during viral infections. These projects aim to identify and target the new kinase or enzymes in macrophages to reduce the pathophysiology of severe sepsis or the development of liver tumours. In this talk, I will summary our findings about the role of VEGFR-3 (Vascular endothelial growth factor receptor-3), STK4 (Ser/Thr-protein kinase 4, also named MST1), HRD1 (HMG-CoA reductase degradation protein 1)and DHCR7 (7-Dehydrocholesterol Reductase) in the innate responses against infection.