Jeri-Anne Lyons, Ph.D.

Associate Professor, Interim Associate Dean for Graduate Studies & Research

[Image] Jeri-Anne Lyons

Enderis Hall, Room 819
Phone: (414) 229-4878
Fax: (414) 229-2206


Biomedical Sciences, Office of Graduate Studies & Research


  • Ph.D., Department of Microbiology, Medical College of Wisconsin, 1997
  • B.S., Medical Technology, University of Wisconsin-Stevens Point, 1989

Speaker Topics

  • Immunology
  • Multiple Sclerosis
  • Phototherapy

Interests & Expertise

Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). It is thought to result from an immune-mediated attack of CNS myelin by autoreactive T cells specific for myelin components. My research focuses on the immunopathogenesis of MS and in identifying novel targets for disease. Studies are performed on cells isolated from MS patients and in a mouse model of MS called Experimental Autoimmune Encephalomyelitis (EAE). In particular, the role of B cells and antibody in disease pathogenesis are of interest. Also of interest is the regulation of immune cell activation. Recent studies have focused on a novel therapeutic approach using red led to stimulate repair pathways, termed “Photobiomodulation”. A variety of cellular and molecular techniques are used to study these questions.

Recent Publications

Liu, G., Muili, K. A., Agashe, V. V. & Lyons, J. A. (2012). Unique B cell responses in B cell-dependent and B cell-independent EAE. Autoimmunity, 45, 199-209.

Muili, K. A., Gopalakrishnanm, S., Meyer, S. L., Eells, J. T., & Lyons, J. (2012). Amelioration of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice by Photobiomodulation Induced by 670 nm Light, PLoS ONE, 7(1), e30655.

Liu, G., Muili, K. A., Agashe, V. V., & Lyons, J. A. (in press). Unique B cell responses in B cell-dependent and B cell-independent EAE. Autoimmunity.

Piccio, L., Naismith, R. T., Trinkaus, K., Klein, R. S., Parks, B. J., Lyons, J. A., & Cross, A. H. (2010). Changes in B- and T-Lymphocyte and Chemokine Levels With Rituximab Treatment in Multiple Sclerosis. Archives of Neurology, 67, 707-714.

Klawiter, E. C., Piccio, L., Lyons, J. A., Mikesell, R., O’Connor, K. C., & Cross, A. H. (2010). Elevated Intrathecal Myelin Oligodendrocyte Glycoprotein Antibodies in Multiple Sclerosis. Archives of Neurology, 67(9), 1102-1108.

Lyons, J. A., Haring, J. S., & Biga, P. R. (2010). Myostatin Expression, Lymphocyte Population, and Potential Cytokine Production Correlate with Predisposition to High-Fat Diet Induced Obesity in Mice. PLoS ONE, 5(9), e12928.

Monson, N. L., Cravens, P., Hussain, R., Harp, C. T., Cummings, M., de Pilar Martin, M., Ben, L., Do, J., Lyons, J. A., Lovette-Racke, A., Cross, A. H., Racke, M. K., Stüve, O., Shlomchik, M., & Eagar, T. N. (2010). Rituximab Therapy Reduces Organ-Specific T Cell Responses and Ameliorates Experimental Autoimmune Encephalomyelitis. PloS ONE: 10.1371/journal.pone.0017103

Naismith, R. T., Piccio, L., Lyons, J. A., Lauber, J., Tutlam, N. T., Parks, B. J., Trinkaus, K., Song, S. K., & Cross, A. H. (2010). Rituximab Add-On Therapy For Breakthrough Relapsing Multiple Sclerosis: a 52-Week Phase II Trial. Neurology, 74(23), 1860-7.

Lyons, J.-A., Ramsbottom, M. J., Mikesell, R. J., & Cross, A. H. (2008). B cells limit epitope spreading and reduce severity of EAE induced with PLP peptide in BALB/c mice. J. Autoimmunity, 31, 149-155. DOI 10.1016/j.jaut.2008.04.025.