Associate Professor of Medicine
- MD, Shandong University, 1987
- MS, Shandong University, 1990
- PhD, University of North Carolina at Chapel Hill, 2004
- Leukocyte migratin in inflammation
- Myeloid cell function in inflammation and autoimmunity
- Rheumatoid arthritis
- Atherosclerosis and vascular inflammation
The primary role of the immune system is to protect tissues from damage by danger signals. However, sustained and uncontrolled immune responses result in inflammatory diseases. Excessive recruitment of immune cells, such as macrophages, dendritic cells, and T cells, to inflamed tissues is one of the major causes of tissue damage. My research interest is to study the regulation of immune cell migration and function in the context of inflammatory diseases such as atherosclerosis and autoimmune arthritis.
Chemokine and chemokine receptors are key regulators of leukocyte trafficking. One of the major precursors of dendritic cells and macrophages is monocytes that express chemokine receptors CX3CR1 and CCR2. We and other researchers have demonstrated that animals that are deficient in either receptor are less susceptible to atherosclerosis. We have also observed that an alteration of dendritic cell numbers in the arterial wall is related to CX3CR1 and CCR2. Further investigation of mechanisms by which CX3CR1 and CCR2 regulate vascular recruitment of dendritic cells and their contributions to atherosclerosis is one of the ongoing projects.
The second major project is to study whether CX3CR1 and CCR2 also play a role in the pathogenesis of autoimmune arthritis, in particular, antigen presentation, T cell differentiation and cytokine production, in animal models of autoimmune arthritis. The ultimate goal of our research is to contribute to an in-depth understanding of disease mechanisms and the possibility of new therapeutic targets in atherosclerosis and arthritis.