|Appointment(s) and Titles:
|Associate Professor, Medical Microbiology and
Associate Professor of Medicine
|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.