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Training
- B. Sc. , 1982: Nanjing Normal University, China
- M.Sc.,1983: Columbia University, New York
- M.Phil., 1985: Columbia University, New York
- Ph. D., 1988: Columbia University, New York
- Postdoctoral Training: Rockefeller University 1988-1991
Positions
- Professor, 2004- present: Microbiology and Immunology, Walther Oncology Center, Indiana University School of Medical at Indianapolis, IN
- Associate Professor, 1997 – 2003:Department of Pathology, Yale University School of Medicine, New Haven, CT
- Professor and Director 2000 - 2001(sabbatical leave): Tsinghua Institute of Genome Research (TIGR in China) Tsinghua University, Beijing China
- Assistant Professor, 1994 –1996:Department of Pathology, Yale University School of Medicine, New Haven, CT
- Assistant Professor, 1992 –1994:Department of Biochemistry, Mount Sinai School of Medicine, New York
Summary of Dr. Fu’s Research Focus
We are focusing on studies of the STAT signaling pathway in regulation of inflammation, innate, adaptive immunity, development and body homeostasis.
Description and summary of research focus of the laboratory:
Dr. Fu’s lab works on the STAT proteins. Recently, we have revealed critical functions of STAT proteins in inflammation, innate & adaptive immunity and body homeostasis. In particular, we have shown STAT3 is an essential regulator of inflammation and immune responses: Loss of STAT3 may lead to Crohn’s disease-like phenotypes, endothelial-mediated sepsis, inflammation-induced heart failure. We have also shown STAT3 in brain controls obesity and glucose metabolism. Our current research efforts are: 1) Molecular mechanisms of STAT3 in negative regulation of innate immunity and inflammation. We will use STAT3 knock-out mice as an animal model system for these studies. We will search for the genes regulated by STAT3 that inhibit innate immunity. These studies should shed light on a novel aspect of innate immunity regulation and provide a new understanding of human inflammatory diseases involving innate immunity. 2) Cytokines and inflammation have emerged as one of the most important factors involved in the development of chronicle congestive heart failure (CHF). To study inflammation and its role in CHF, we will utilize cardiomyocyte specific STAT3 KO mice we have generated to reveal critical regulatory mechanisms during pathogenesis of inflammation-induced CHF. 3). Autoimmune diseases are complex syndromes of self-destruction caused by disorders not only in adaptive immune responses but also in innate immune responses. The major cause of autoimmune disease is loss of immune tolerance. We are interested in the molecular mechanisms by which immune tolerance is regulated. Our recent data suggest that loss of STAT3 causes a cascade of events that affect dendritic cell (DC) differentiation, abnormal generation of inflammatory cytokines, polarized Th1 activation, B cell over-proliferation and eventually lead to autoimmune disorders similar to systemic lupus erythematosus (SLE). Surprisingly, DC-elimination in STAT3 deficient mice did not cause immunodeficiency, but lead to autoimmune diseases in these mice, suggesting the indispensable function of DC is regulation of immune tolerance. With the unique animal models generated in our lab, we will further investigate molecular mechanisms controlling DC differentiation and search for mechanisms by which STAT3 regulates immune tolerance. These studies will further reveal molecular mechanisms on how STAT proteins control immune responses and inflammation.
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