上海交通大学“盛毓绶”冠名讲席教授，中组部“千人计划”入选者。1987年获英国爱丁堡大学分子遗传学专业博士学位，先后在美国宾夕法尼亚大学担任高级研究员、康奈尔大学担任终身教授，长期从事探索免疫学领域的基础研究，在揭示免疫反应细胞和分子作用机制及开创新的探测技术方法手段方面取得了突出成绩。在Nature Immunology、Immunity、J. Experimental Medicine, J.Immunology等高水平国际期刊杂志发表SCI论文103篇，他引次数达10125次。2014-2017年度连续四年被Elsevier列为中国医学类最高被引用研究者之一。相关研究成果的独特与创新性被Nature和Cell、Nature Reviews Immunology等进行专题报导和评论。曾荣获Young Investigators Award by International Cytokine Society、Howard Temin Award (NCI/NIH)等奖励。
MOLECULAR MECHANISMS OF cytokine GENE EXPRESSION and their immunological activities IN inflammatory diseases
Interleukin-12 (IL-12) is a heterodimeric, proinflammatory cytokine produced by phagocytic cells and plays a critical role in the activation and function of antigen-presenting cells and effector lymphocytes during microbial infection. Interleukin-10 (IL-10) is a homodimeric cytokine produced mainly by monocytes/macrophages, activated T and B lymphocytes. IL-10 has potent anti-inflammatory and immunosuppressive activities on myeloid cell functions while it also exerts immune stimulatory effects on B cells for proliferation, differentiation and antibody production. It is a pivotal homeostatic regulator of immune reactivity. The production of IL-12 and IL-10 by phagocytic and antigen-presenting cells is regulated in opposite manners during innate and adaptive immune responses. The understanding of the molecular mechanisms controlling the gene expression of IL-12 and IL-10 in interactions between pathogens and the immune system is essential to efforts to develop therapeutic strategies for infectious, malignant and autoimmune diseases. We are currently investigating in the following areas:
I. Molecular mechanism of the regulation of IL-23 gene expression during phagocytosis of apoptotic cells by macrophages and dendritic cells, and its impact on the development of Th17 cells in lupus.
II. Molecular mechanisms of the regulation of IL-12 gene expression in APCs by the Crohn’s disease-associated mutants of nucleotide-binding oligomerization domain 2 (Nod2) and IL-12-mediated inflammatory bowel disease.
III. Molecular and cellular mechanisms whereby cancer cell-derived novel molecules inhibits dendritic cell-induced T cell activation and T cell-mediated antitumor immunity.
IV. Role and mechanism of CCL5 in the development of myeloid-derived suppressor cells in triple negative breast cancer.
V. Control of inflammation by progranulin through regulation of IL-10 production in sepsis and in the central nervous system.
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