Hubert M. Tse, PhD

Chair, Microbiology, Molecular Genetics and Immunology
htse@kumc.eduMore:
Professional Background
Hubert Tse completed his undergraduate studies in Biochemistry at Virginia Tech (B.S., 1992). He performed his graduate work on M. xanthus differentiation with Dr. Ronald E. Gill in the Department of Microbiology and Immunology at the University of Colorado Health Sciences Center. He obtained his Ph.D. in Microbiology and Immunology in 1999 and went on to a post-doctoral fellowship in Dr. Andrea Cooper’s group at Colorado State University in Ft. Collins, CO studying macrophage responses following M. avium infection. In 2001, he went and did a second post-doctoral immunology fellowship in Dr. Jon Piganelli’s group at the University of Pittsburgh studying the autoimmune mechanisms involved in pancreatic beta-cell destruction in Type 1 diabetes. In 2009, he moved to the University of Alabama at Birmingham (UAB), and started his own research lab. Over the next 13 years, Dr. Tse developed research programs studying genetics, innate immune (macrophage, dendritic cell), adaptive immune (CD4 and CD8 T cell), and beta-cell responses involved in Type 1 diabetes and islet transplantation rejection. In 2023, Dr. Tse and his lab was recruited to KUMC. Dr. Tse is currently serving as the Professor and Chair of the Department of Microbiology, Molecular Genetics, and Immunology. He is also affiliated with the Diabetes Institute at KUMC to foster additional research programs on Type 1 diabetes.
Education and Training
- BS, Biochemistry, Virginia Tech, Blacksburg, VA
- Post Doctoral Fellowship, Host Defense, Colorado State University, Ft. Collins, CO
- Post Doctoral Fellowship, Autoimmunity, University of Pittsburgh, Pittsburgh, PA
Research
Overview
Our research objective is to define and prevent immune-mediated effector mechanisms involved in the destruction of insulin-producing pancreatic beta-cells in Type 1 diabetes (T1D) and islet transplantation. Specifically, we are interested in determining how oxidative stress can regulate innate and adaptive immune responses. We previously demonstrated that Non-Obese Diabetic (NOD) mice lacking the ability to generate NADPH oxidase-derived superoxide exhibited a significant delay in spontaneous, adoptive transfer, and virus-accelerated T1D. Our research has shown a synergistic interaction between redox biology and dysregulated autoimmune responses, specifically, the activation of signaling pathways necessary to mature CD4+ and CD8+ T cell effector responses and promote inflammatory macrophage differentiation in T1D are redox-regulated. Currently, we continue to characterize the redox-dependency of antiviral responses following diabetogenic Coxsackievirus infections, the role of thiol-dependent signaling on autoreactive T cells, why genetic susceptibility genes influence autoimmunity, and the efficacy of islet encapsulation to delay allo- and xenograft rejection in mouse models and human translational studies in T1D.