Harley Y. Tse, Ph.D., is a Professor and Deputy Chair in the Department of Immunology and Microbiology. He joined the Department in 1986. Dr. Tse received his B.S. With Honors from the California Institute of Technology in 1972. He did his graduate work at the University of California, San Diego and received his Ph.D. in Immunology in 1977. From 1977 to 1980, Dr. Tse was trained in Immunogenetics in the laboratories of Dr. William Paul and Dr. Ronald Schwartz at the National Institutes of Health. He was employed as a Senior Research Immunologist in the Department of Immunology at the Merck Sharp and Dohme Research Laboratories of Merck & Company. Dr. Tse was a recipient of the NIH Research Career Development Award from 1992 to 1997. He has also served as regular members of several NIH study sections over the last 20 years, including Immunological Sciences (IMS), Hypersensitivity, Autoimmune and Immune-mediated Diseases (HAI), Clinical Immunology and Brain Tumors (CNBT) and National Center for Complementary and Alternative Medicine (NCCAM) study sections .
Dr. Tse's research emphasis is in autoimmunity and autoimmune diseases. His laboratory uses an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE) to study immune regulation of the central nervous system (CNS). He constructed a Thy-1 congenic mouse strain on the SJL background, SJL.Thy-1a, to track the trafficking of pathogenic T cells from the lymphoid organ to the CNS. His laboratory developed a novel experimental model to induce EAE in traditional non-responder mouse strains, thus suggesting that EAE unresponsiveness was not due to genetic factors, but to regulatory mechanisms such as regulatory T cells (Tregs). Using adoptive transfer and neonatal tolerance techniques, Dr. Tse also showed that EAE resistance was not associated with the permeability of the blood-brain-barrier and entry of pathogenic T cells into the CNS. Current research aims at elucidating how Tregs control the development of the paralytic disease.
Another area of research in Dr. Tse's laboratory is understanding how immune T cells regulate the development of atherosclerosis, a precursor of cardiovascular diseases such as heart attack and strokes. In collaboration with Dr. Michael Shaw of the St. John-Providence Health System, they have identified the first antigenic epitope of ApoB-100, P6, that exacerbate formation of atherosclerotic plaques in the aortas. Using T cell cloning techniques, Dr. Tse has generated a panel of P6-specific T cell clones that when, adoptively transferred into naive recipients, enhanced the development of atherosclerosis. This is the first time that a homogeneous population of atherogenic T cells is available for functional studies. Current research aims at developing a T cell receptor transgenic mouse strain for studying the functional roles of each of the T cell subpopulations, especially Tregs.
Office Location8245 Scott Hall
- Skundric, DS., Cruikshank, WW., Montgomery, PC., Lisak, RP. and Tse, HY. 2015. Emerging role of IL-16 in cytokine-mediated regulation of multiple sclerosis. Cytokine. 75:234-248. doi: 10.1016/j.cyto.2015.01.005. PMID: 25703787 (Paper selected for publication of Abstract in Global Medical Discovery journal: https://globalmedicaldiscovery.com/key-scientific-article /emerging-role-of-il-16-in-cytokine-mediated-regulation-of-multiple-sclerosis/)
- Skundric, DS., Tuzova, MN., Cruikshank, WW., Montgomery, PC., and Tse, HY. 2015. Current concepts of interleukin-16 (IL-16) in the onset and progression of multiple sclerosis. In “Innovative Immunology”, Khan, WA., Editor. Austin Publishing Group/eBook, pp1-17. http://austinpublishinggroup.org/ebooks/innovative-immunology/index.php
- Shaw, MK., Welch, K., Zhao, X., Montgomery, PC., Thummel, R., and Tse, HY. 2014. Identification of Two Immunologic T Cell Epitopes of ApoB-100 and Their Autoimmune Implications. J. Immunol. & Clin. Res. 2(2):1021.
- Tatar, C., Bessert, D., Tse, H. and Skoff, R.P. 2013. Determinants of central nerve system adult neurogenesis are sex, hormones, mouse strain, age and brain region. Glia. 61:192-209, PMID: 23027402.
- Tse, H.Y., Skundric, D.S., Cruikshank, W.W., Montgomery, P.C. and Lisak, R.P. 2013 Immunopathology of CD4+ T cell-mediated autoimmune responses to central nervous system antigens: Role of IL-16. J. Immunol. & Clin. Res. 1:1005.
- Tse, K., Tse, H., Sidney, J., Sette, A. and Ley, K. 2013. T cells in atherosclerosis. Int. Immunol. 25:615-622, 2013.
- Tse, K., Gonan, A., Sidney, J., Ouyang, H., Witztum, J., Sette, A., Tse, H., and Ley, K. 2013. Atheroprotective Vaccination with MHC-II Restricted Peptides from ApoB-100. Frontiers in Immunotherapies and Vaccines. 4:493, 2013. PMID: 24416033
- Shaw, M.K., Li, J., Zhao, X., Ho, P.P. and Tse, H.Y. 2012. Natural resistance to induction and development of experimental autoimmune encephalomyelitis. Curr. Trends in Immunol. 13:1-12.
- Shaw, M.K., Zhao, X, and Tse, H.Y. 2012. Overcoming unresponsiveness in EAE resistant mouse strains by adoptive transfer and antigenic challenge. J. Vis. Exp. (62), e3778, DOI:10.3791/3778.
- Li, J., Zhao, X., Skoff, R., Shaw, M.K. and Tse, H.Y. 2011. Differential levels of resistance to disease induction and development of relapsing experimental autoimmune encephalomyelitis in two H-2b-restricted mouse strains. J. Neuroimmunol. 234:109-114,
- Li, J., Zhao, X, Hao, H-W., Shaw, M.K. and Tse, H.Y. 2011. T cells that trigger acute experimental autoimmune encephalomyelitis also mediate subsequent disease relapses and predominantly produce IL-17. J. Neuroimmunol. 230:26-32, 2011