Jeri-Anne Lyons, Ph.D.
Associate Professor, Biomedical Sciences Graduate Coordinator, Chair
- Clinical Chemistry
- Multiple Sclerosis
Enderis Hall, Room 417
Phone: (414) 229-3812
Fax: (414) 229-2619
- Ph.D., Department of Microbiology, Medical College of Wisconsin, 1997
- B.S., Medical Technology, University of Wisconsin-Stevens Point, 1989
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.
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.
Nancy L Monson, Petra Cravens, Rehana Hussain, Christopher T Harp, Matthew Cummings, Maria de Pilar Martin, Li-Hong Ben, Julie Do, Jeri-Anne Lyons, Amy Lovette-Racke, Anne H Cross, Michael K Racke, Olaf Stüve, Mark Shlomchik, Todd N Eagar. 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. Rituximab Add-On Therapy For Breakthrough Relapsing Multiple Sclerosis: a 52-Week Phase II Trial. Neurology, 74(23), 1860-7, 2010 Jun 8.
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.
Cross, A.H., Stark, J.L., Lauber, J., Ramsbottom, M,J., & Lyons, J.-A. (2006). Rituximab reduces B cells and T cells in Cerebrospinal Fluid of Multiple Sclerosis Patients. J. Neuroimmunology, 180, 63-70.
Cross, A.H., Ramsbottom, M.J., & Lyons, J.A. (2006). NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis. J. of Neuroimmunology, 173, 79-86.
Stark, J.L., Lyons, J.A., & Cross, A.H. (2004). Interferon-gamma produced by encephalitogenic cells induces suppressors of cytokine signaling (SOCS) in primary murine astrocytes. J. Neuroimmunology, 151, 195-200.
Lyons, J.-A., Ramsbottom, M.J., Trotter, J.L., & Cross, A.H. (2002). Identification of the encephalitogenic epitopes of CNS proteolipid protein in Balb/c mice. J. Autoimmunity, 19, 195-201.
Lyons, J.-A., Ramsbottom, M.J., & Cross., A.H. (2002). Critical role of antigen-specific antibody in EAE induced by recombinant MOG. European J. Immunology, 32, 1905-1913.Back to the top
Lyons, J.A., & Cross, A.H. (2005). Endothelial cells and adhesion molecules in experimental autoimmune encephalomyelitis. In E. Lavi & C. Constantinescu (Eds.), Experimental models of MS (pp. 151-179). Springer, New York.
Lyons, J.-A. (2003). The Role of CD1-mediated presentation of myelin lipids in MS pathology. Drug News and Perspectives, 16, 574-584.
Cross, A.H., Trotter, J.L., & Lyons, J.-A. (2001). B cells and antibodies in CNS demyelinating disease. J. Neuroimmunol, 112, 1-14.
Cross, A.H., Lyons, J.-A., & Trotter, J.L. (2000). Autoantibodies in Demyelinating Disease. In S. Cook (Ed.), Multiple Sclerosis. Marcel Dekker, New York.