Our lab is focused on understanding the regulation of the innate immune response to pathogenic infection and tissue damage. Innate immunity is the first line of host defense that prevents infection and eliminates microbes. In addition, innate immunity plays a pivotal role in the initiation and determination of the adaptive immune response. Innate immune cells, such as macrophages, use pattern-recognition receptors (PRRs) to detect conserved microbial molecules termed pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) released by injured cells to induce pro-inflammatory cytokines, chemokines, interferons and upregulate co-stimulatory molecules. Apart from the beneficial effects of pro-inflammatory cytokines in promoting inflammatory cell accumulation and stimulating the antimicrobial system, an imbalance between pro- and anti-inflammatory cytokines might contribute to the pathogenesis of chronic inflammatory and infectious diseases. As such, the innate immune response must be tightly regulated to avoid uncontrolled inflammation. We have utilized various approaches that include molecular and cellular studies, and mouse genetic models to address our research questions. Our current research interests are aimed at elucidating 1) Regulatory mechanisms of inflammatory responses and inflammatory cell deaths; 2) Crosstalk between innate and adaptive immunity; 3) Mechanisms and functions of macrophage polarization and tumor-associated macrophage.
