Ruolan Liu, M.D., Ph.D.

Ruolan Liu, M.D., Ph.D.

Ruolan Liu


Assistant Professor

Medical Dental Research Building #542
University of Louisville School of Medicine
Louisville, KY 40202
Phone: 502-852-312


Education

MD Shanghai Medical College, Fudan University, Shanghai, China

PhD Neuroscience Program, University of Southern California, Los Angeles, California

MS Applied Biometry & Epidemiology, University of Southern California, Los Angeles, California

Biography

Dr. Liu received her MD degree from the Shanghai Medical University (now the Shanghai Medical College of Fundan University) in Shanghai, China. She further obtained her PhD degree in Neuroscience and her MS degree in Biostatistics at the University of Southern California. She joined the Department of Neurology at the Barrow Neurological Institute to study immunoregulations in autoimmune neurological disorders. Her work has been supported by a 3-year Career Development Grant award from the Muscular Dystrophy Association. She joined the faculty of the University of Louisville, School of Medicine in 2011.

Research Interests

Immune cells and Immune mediators influence the initiation and progression of specific neurological diseases, including myasthenia gravis (MG), multiple sclerosis (MS), stroke and Alzheimer’s disease (AD). To better understanding the cross interactions among the nervous and immune systems during development, homeostasis, and response to injuries, Dr. Liu is interested in the mechanisms of regulatory immune cells (i.e., CD4+CD25+ regulatory T cells and NK cells) in autoimmune neurological diseases (i.e., MS, MG, NMO) and other neurological disorders with an inflammatory component (i.e., Stroke, AD, brain trauma) in both animal models and human subjects. She is also interested in translating bench research findings into new immunotherapy strategies.

Selected Publications

Liu R, Liu W, Doctrow S, Baudry M. (2003) Iron Toxicity in Organotypic Cultures of Hippocampal Slices: Role of Reactive Oxygen Species. J Neurochem 85: 492-502.

Liu R, Liu IY, Bi X, Thompson RF, Doctrow, S, Malfroy B, Baudry M. (2003) Reversal of Age-Related Learning Deficits and Brain Oxidative Stress with Superoxide Dismutase/Catalase Mimetics.  ProcNatlAcadSci USA 100: 8526-31.

Liu R, La Cava A, Campagnolo D, Price M, Vollmer L, Van Kaer L & Shi FD.(2005) Cooperation of iNKT Cells and CD4+CD25+Treg Cells in the Prevention of Autoimmune Myasthenia. J Immunol 175:7898-7904.

Liu R, Van Kaer L, La Cava A, Price M, Rhodes S, Campagnolo DI, Vollmer TL, and Shi FD. (2006) Autoreactive T Cells Mediate NK Cell Degeneration in Autoimmune Disease. J  Immunol176:5247-5254.

Liu R, Bai Y, Vollmer TL, Bai XF, Jee Y, Tang Y, Campagnolo DI, Collins M, Young DA, La Cava A, and Shi FD. (2008) IL-21 Receptor Expression Determines the Temporal Phases of Experimental Autoimmune Encephalomyelitis. ExpNeurol 211:14-24.

Liu R*, Hao JW, Daoyao CS, Vollmer TL, Shi FD, and Campagnolo DI*. (2009) Transcriptional factor T-bet influences the helper and regulatory T cells the susceptibility to experimental myasthenia gravis. ExpNeurol220:366-373. (*Corresponding authors)

Liu R*, Hao JW, and Shi FD* (2010).“Regulatory T cells in myasthenia”. In Myasthenia gravis: Disease mechanisms and immune intervention. P. Christadoss, eds. Linus Publications, Inc. (ISBN 978-1-60797-060-6). (*Corresponding authors)

Liu R*, Zhou Q, La Cava A, Campagnolo DI, Van Kaer L, and Shi FD*. (2010) Expansion of regulatory T cells via IL-2/anti-IL-2 mAb complexes suppresses eperimental myasthenia. Eur J  Immunol40:1577-1589. (*Corresponding authors)

Hao JW*, Liu R*, Piao WH*, Zhou QH, Vollmer TL, Campagnolo DI, Xiang R, La Cava A, Van Kaer L, and Shi FD. (2010) Central nervous system (CNS)-resident NK cells suppress Th17 responses and CNS autoimmune pathology. J Exp Med 207:1907-1921.(*co-1st authors)

Hao JW, Campagnolo DI, Liu R, Piao WH, Shi S, Hu B, Xiang R, Zhou Q, Vollmer T, Van Kaer L, La Cava A, and Shi FD. (2011) Interleukin-2/interleukin-2 antibody therapy induces target organ nature killer cells that inhibit central nervous system inflammation. Ann Neurol 69:721-734.