Dean T. Nardelli, Ph.D.

Assistant Professor, Graduate Program Coordinator

[Image] Dean Nardelli

Enderis Hall, Room 493
Phone: (414) 229-6362
Fax: (414) 229-2619
nardelld@uwm.edu

Department

Biomedical Sciences

Education

  • Ph.D., Comparative Biomedical Sciences, University of Wisconsin-Madison, 2007
  • M.S., Bacteriology, University of Wisconsin-Madison, 2003
  • B.S., Medical Microbiology & Immunology, University of Wisconsin-Madison, 2000


Speaker Topics

  • Immunology
  • Microbial Pathogenesis
  • Lyme Disease

Interests & Expertise

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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. We are 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. We are also investigating how later-stage disease symptoms affect, and are affected by, the host’s response to infection.


Recent Publications

Hansen, E. S., Medić, V., Kuo, J., Warner, T. F., Schell, R. F., & Nardelli, D. T. (2013). IL-10 Inhibits Borrelia burgdorferi-Induced IL-17 Production and Attenuates IL-17-Mediated Lyme Arthritis. Infect. Immun. Epub ahead of print Sep. 16, doi:10.1128/IAI.01129-13

Munson, E., Nardelli, D. T., Du Chateau, B. K., Callister, S. M., & Schell, R. F. (2012). Hamster and Murine Models of Severe Destructive Lyme Arthritis. Clinical and Developmental Immunology, [Online], Vol. 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. Clinical and Vaccine Immunology, 18 (7), 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. Microbiology, 60(1), 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, 457-469.

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, 1199-1207.

Nardelli, D. T., Luk, K. H. K., Kotloski, N. J., Warner, T. F., Torrealba, J. R., Callister, S. M., & Schell, R. F. (2008). Role of IL-17, transforming growth factor-ß, 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, 265-274.

Nardelli, D. T., Callister, S. M., & Schell, R. F. (2008) Lyme arthritis: current concepts and a change in paradigm. Clin. Vaccine Immunol, 15, 21-24.


Presentations

“Regulation of Interleukin-17 in Borrelia burgdorferi-Induced Arthritis”; Medical College of Wisconsin Infectious Disease Research Conference Series, August 1, 2013, Milwaukee, WI.

“Gram-Negative Anaerobes”; University of Wisconsin-Madison Department of Medical Microbiology and Immunology, April 1, 2013, Madison, WI.

“Lyme Disease: The Science and the Controversies”; Concordia University School of Pharmacy, March 20, 2013, Mequon, WI.

“Gram-Negative Anaerobes”; University of Wisconsin-Madison Department of Medical Microbiology and Immunology, March 23, 2012, Madison, WI.

“Novel Mechanisms of Lyme Arthritis”; Department of Kinesiology, University of Wisconsin-Milwaukee, February 21, 2012, Milwaukee, WI.


Affiliations

  • Editorial Board, ISRN Infectious Diseases

Professional Memberships

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

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