Faculty Information
Kristen M. Drescher, Ph.D.
Appointment & Titles | Research Interests  | Selected Publications  |  Contact

Appointment(s) and Titles:
Associate Professor, Medical Microbiology and Immunology
Associate Professor of Medicine
Research Interests:
Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS) in humans. Patients with MS normally experience a chronic progressive loss of motor and/or sensory functions. The origin of MS is unknown, although some investigators have postulated than an environmental agent (i.e. a virus or bacteria) may trigger the disease. My laboratory utilizes a mouse model of virus-induced demyelination (Theiler's murine encephalomyelitis virus) to study immune factors involved in the development of pathology and clinical disease.

Selected Publications:
Drescher, K.M., Pease, L.R., and Rodriguez, M. (1997). Antiviral immune responses modulate the nature of central nervous system (CNS) disease in a murine model of multiple sclerosis. Immunol Reviews 159: 177-193.

Drescher, K.M., Nguyen, L.T., Coenen, M.J., Leibowitz, J.L., Strauss, G., Hammerline, G.J., David, C.S., and Rodriguez, M. (1998). Expression of the human HLA-DR3 transgene reduces the severity of demyelination in a murine model of multiple sclerosis. J Clin Invest 101: 1765-1774.

Drescher, K.M., Murray, P.D., David, C.S., Pease, L.R. and Rodriguez, M. (1999). CNS cell populations are protected from virus-induced pathology by distinct arms of the immune system. Brain Pathol 9: 21-31.

Drescher, K.M., Zoecklein, L.J., Pavelko, K.D., Rivera-Quinones, C., Hollenbaugh, D. and Rodriguez, M. (2000) CD40L is critical for protection from demyelinating disease and development of spontaneous remyelination in a mouse model of multiple sclerosis. Brain Pathology 9: 1-15.

Drescher, K.M., Murray, P.D., Lin, X., Carlino, J. and Rodriguez, M. (2000) TGFB reduces demyelination, virus antigen expression, and macrophage recruitment in a viral model of multiple sclerosis. J Immunol 164: 3207-3213.

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