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Dean T. Nardelli, PhD

Associate Professor, Graduate Program Coordinator

Education

Post-Doctoral Immunology University of Wisconsin-Madison, Wisconsin State Labratory of Hygiene 2009
Ph D Comparative Biomedical Sciences University of Wisconsin-Madison 2007
MS Bacteriology University of Wisconsin-Madison 2003
BS Medical Microbiology and Immunology University of Wisconsin-Madison 2000

Interests & Expertise

Dean Nardelli’s research looks at arthritis as frequent manifestation of Lyme Disease. Lyme borreliosis, caused by infection with the bacterium Borrelia burgdorferi, is the most common tick-borne disease in North America. It is a multi-stage inflammatory disease that affects several body systems, leading to significant morbidity in untreated individuals.

Arthritis is among the most frequent pathological manifestations of later-stage Lyme borreliosis and, in a subset of genetically predisposed individuals, persists even after completion of antibiotic therapy.

One hypothesis to explain this phenomenon is the development of autoimmunity following infection with B. burgdorferi. In order to reduce morbidity in individuals with later-stage manifestations of Lyme borreliosis, it is imperative to understand the immune factors that contribute to disease. Cells of the adaptive immune response (T cells, specifically) are considered to play a significant role in the development of later-stage Lyme arthritis.

His is investigating the host and microbial factors that lead to the induction of different T cell subsets that are responsible for the development, progression, resolution and, potentially, prevention of Lyme arthritis. He is also investigating how later-stage disease symptoms affect, and are affected by, the host’s response to infection.

Selected Publications

Kuo, J., Warner, T. F., Munson, E. L., Nardelli, D. T., & Schell, R. F. (2016, October (4th Quarter/Autumn)). Arthritis is developed in Borrelia-primed and -infected mice deficient of interleukin-17. van Eden, W. (Ed.). Pathogens and Disease, 74(7), ftw077.
Hansen, E. S., Johnson, M. E., Schell, R. F., & Nardelli, D. T. (2016, October (4th Quarter/Autumn)). CD4+ cell-derived interleukin-17 in a model of dysregulated, Borrelia-induced arthritis. Marconi, R. (Ed.). Pathogens and Disease, 74(7), ftw084.
Hansen, E. S., Medic, V., Kuo, J., Warner, T. F., Schell, F., & Nardelli, D. T. (2013). IL-10 inhibits Borrelia burgdorferi-induced IL-17 production and attenuates IL-17-mediated Lyme arthritis. Infect. Immun, 81(12), 4421-4430.
Munson, E., Nardelli, D. T., Du Chateau, B., & Callister, S. M. (2012). Hamster and Murine Models of Severe Destructive Lyme Arthritis. Clin. Develop. Immunol, 2012.
Kuo, J., Nardelli, D. T., Warner, T. F., Callister, S. M., & Schell, R. F. (2011). Interleukin-35 enhances Lyme arthritis in Borrelia-vaccinated and infected mice. Clin. Vaccine Immunol, 18, 1125-1132.
Nardelli, D. T., Luedtke, J. O., Munson, E. L., Warner, T. F., Callister, S. M., & Schell, R. F. (2010). Significant differences between the Borrelia-infection and Borrelia-vaccination and -infection models of Lyme arthritis in C3H/HeN mice. FEMS Immunol Med Microbiol, 60, 78-89.
Nardelli, D. T., & Schell, R. F. (2009). Expanded role for IL-17 in Lyme arthritis. 60, 1202.
Nardelli, D. T., Munson, E. L., Callister, S. M., & Schell, R. F. (2009). Human Lyme Disease Vaccines: Past and Future Concerns. Future Microbiol, 4(4), 457-469.
Nardelli, D. T., Luk, K. H., Kotloski, N. J., Warner, T. F., Torrealba, J. R., Callister, S. M., & Schell, R. F. (2008). Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-OspA borreliacidal antibodies in Borrelia-vaccinated and challenged mice. FEMS Immunol Med Microbiol, 53, 265-275.
Nardelli, D. T., Callister, S. M., & Schell, R. F. (2008). Lyme arthritis: current concepts and a change in paradigm. Clin Vaccine Immunol, 15(1), 21-24.
Kotloski, N. J., Nardelli, D. T., Peterson, S. H., Torrealba, J. R., Warner, T. F., Callister, S. M., & Schell, R. F. (2008). Interleukin (IL)-23 is required for the development of arthritis in mice vaccinated and challenged with Borrelia species. Clin. Vaccine Immunol, 15(8), 1199-1207.
Peterson, S. H., Nardelli, D. T., Warner, T. F., Callister, S. M., Torrealba, J. R., & Schell, R. F. (2007). Anti-p19 antibody exacerbates Lyme arthritis and enhances borreliacidal activity. Clin Vaccine Immunol, 14, 510-517.
Nardelli, D. T., Warner, T. F., Callister, S. M., & Schell, R. F. (2006). Anti-CD25 antibody treatment of Borrelia-vaccinated and challenged mice does not exacerbate arthritis but inhibits borreliacidal antibody production. Clin Vaccine Immunol, 13(8), 884-891.
Amlong, C. A., Nardelli, D. T., Peterson, S. H., Warner, T. F., Callister, S. M., & Schell, R. F. (2006). Anti-interleukin-15 prevents arthritis in Borrelia-vaccinated and infected mice. Clin Vaccine Immunol, 13, 289-296.
Munson, E. L., Nardelli, D. T., Luk, K. H., Remington, M. C., Callister, S. M., & Schell, R. F. (2006). Interleukin-6 promotes anti-OspA borreliacidal antibody production in vitro. Clin. Vaccine Immunol, 13, 19-25.