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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 Pathobiological Sciences University of Wisconsin-Madison 2007
MS Bacteriology University of Wisconsin-Madison 2003
BS Medical Microbiology and Immunology University of Wisconsin-Madison 2000

Speaker Topics

  • Immunology
  • Microbial Pathogenesis
  • Lyme Disease

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. 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. 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., 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., & Schell, R. F. (2009). Expanded role for IL-17 in Lyme arthritis. Arthritis Rheum, 60, 1202.
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.
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.
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.

Presentations

Nardelli, D. T. (September 2016). Immunoregulatory Mechanisms of Lyme Arthritis. Seminar Series, Rockford, IL.
Nardelli, D. T. (March 2016). Gram-Negative Anaerobes. , Madison, WI.
Hansen, E. S., Liedhegner, E. S., & Nardelli, D. T. (January 2016). Influence of Regulatory T Cells on Host Response to Borrelia burgdorferi. Gordon Research Conference- Biology of Spirochetes, Ventura, CA.
Hansen, E. S., Hillard, C. J., & Nardelli, D. T. (January 2016). Regulation of Lyme Arthritis by Cannabinoid Type 2 Receptor. Gordon Research Conference- Biology of Spirochetes, Ventura, CA.
Nardelli, D. T. (December 2015). The Role of Cannabinoid Receptor 2 (CB2) in Lyme Arthritis. University of Wisconsin-Milwaukee College of Health Sciences Research Symposium, Milwaukee, WI.
Nardelli, D. T. (May 2015). Interferon Gamma is Involved in Borrelia-Induced Arthritis in Mice Lacking Interleukin-17. American Association of Immunologists Annual Meeting, New Orleans, LA.
Nardelli, D. T. (March 2015). Gram-Negative Anaerobes. , Madison, WI.
Nardelli, D. T. (April 2014). Current Concepts in Lyme Disease. American Society for Clinical Laboratory Science-Wisconsin Chapter State Convention, Milwaukee, WI.
Nardelli, D. T. (March 2014). Gram-Negative Anaerobes. University of Wisconsin-Madison Department of Medical Microbiology and Immunology, Madison, WI.
Nardelli, D. T. (March 2014). Immune Regulation of Lyme Arthritis. College of Health Sciences, Milwaukee, WI.
Nardelli, D. T. (January 2014). Regulation of Interleukin (IL)-17 Production and IL-17-Driven Inflammation by IL-10 in a Murine Model of Borrelia-Induced Arthritis. Gordon Research Conference-Biology of Spirochetes, Ventura, CA.
Nardelli, D. T. (December 2013). IL-17 Inhibits IL-10 Production and Lyme Arthritis Following Borrelia burgdorferi Infection. University of Wisconsin-Milwaukee College of Health Sciences Research Symposium, Milwaukee, WI.
Nardelli, D. T. (August 2013). Regulation of Interleukin-17 in Borrelia burgdorferi-Induced Arthritis. Medical College of Wisconsin Infectious Disease Research Conference Series, Milwaukee, WI.
Nardelli, D. T. (May 2013). Regulation of Borrelia burgdorferi-Induced, Interleukin-17-Mediated Inflammation by Interleukin-10. American Society for Microbiology 113th General Meeting, Denver, CO.
Nardelli, D. T. (April 2013). Gram-Negative Anaerobes. University of Wisconsin-Madison Department of Medical Microbiology and Immunology, Madison, WI.

Affiliations

  • Editorial Board, ISRN Infectious Diseases

Professional Memberships

  • Member, American Association of Immunologists
  • Member, American Society for Microbiology

Honors & Awards

Dean’s Award for Outstanding Service (2015) College of Health Sciences, University of Wisconsin-Milwaukee.

Courses Taught

  • * Art of Scientific Communication: BMS 590, 2 cr, G, Department of Biomedical Sciences, University of Wisconsin-Milwaukee (spring 2013)
  • * Infection and Immunity: BMS 750, 3 cr, G; Department of Biomedical Sciences, University of Wisconsin-Milwaukee (fall 2011-2013)
  • Applied Clinical Microbiology: BMS 536, 3 cr, U/G; Department of Biomedical Sciences, University of Wisconsin-Milwaukee (summer 2011-2013)
  • Experimental Design, Research, and Epidemiological Methods: BMS 718, 1 cr, G; Department of Biomedical Sciences, University of Wisconsin-Milwaukee (spring 2011-2013)

*Developed