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Relapses Prevented In Mouse Model Of Multiple Sclerosis: Research Aimed At,,Treating Relapses In Human MS

Researchers at the University of Pennsylvania Medical Center have discovered that antibodies to a common inflammatory-response protein can prevent relapses in an animal model of human multiple sclerosis. "We have been able to prevent relapses in the mouse version of multiple sclerosis using anti-interleukin-12 antibodies for the first time," says Mohamad Rostami, MD, PhD, professor of neurology at Penn's School of Medicine. "Most treatments for MS are first tried out in the experimental allergic encephalomyelitis, or EAE, animal model of MS, before being tested in humans, so this research represents another possible therapy for MS patients." Rostami, Cris Constantinescu, a doctoral student in Rostami's laboratory, and colleagues report their findings in the November 1 issue of the Journal of Immunology.

MS, a neurological disorder, affects 300,000 or more young adults in the United States. Many with the disease suffer from relapses after the initial onset of such symptoms as numbness and paralysis. Trying to remedy these relapses is the research focus of Rostami and his collaborators.

Although the origins of MS remain mysterious, the disorder is considered an autoimmune disease. Immune system cells called T cells cause inflammation in the brain and spinal cord, which is eventually followed by demyelination, the breakdown of the protective sheath that surrounds nerve axons. Certain T cells work in conjunction with proteins called cytokines to cause the damage. "In brains of EAE mice, we saw that the cytokine interleukin-12 is upregulated when there's a relapse and downregulated during a remission," says Rostami. "We believe that both MS and EAE are induced by the Th1 type of T cell. Th2 cells, another type of T cell, are important for recovery from inflammation."

As part of MS-induced inflammation Th2s will try to fight the damage that Th1 cells cause. Rostami reasoned that if the cytokine balance could be changed to decre
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Contact: Karen Young Kreeger
kreeger@mail.med.upenn.edu
215-614-0290
University of Pennsylvania School of Medicine
28-Oct-1998


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