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ShareJan. 4, 2009 — A group led by Dr. Cedric Raine at Albert Einstein College of Medicine have explored the expression of an immune molecule (CXCL1) that interacts with myelin-producing cells, finding that CXCL1 decreases the severity of disease in a mouse model of multiple sclerosis (MS).
The autoimmune disease multiple sclerosis (MS) attacks the central nervous system, resulting in demyelination of neurons. Myelin-producing cells in the central nervous system are severely depleted in lesions in patients with MS.
Myelin-producing cells express immune receptors and have been shown to respond to the immune molecule CXCL1, although the role of CXCL1 in MS has not been previously explored. Dr. Raine and colleagues examined the effects of CXCL1 specifically expressed in the nervous system in a mouse model of MS. They observed decreased severity of disease and more prominent remyelination in these mice. CXCL1, therefore, may play a neuroprotective role in CNS autoimmune demyelination.
In future studies, Dr. Raine's group plans to determine how CXCL1 mediates protection in MS. "Exploration of these pathways affords novel therapeutic avenues to enhance the limited remyelination typically seen in MS."
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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Omari KM, Lutz SE, Santambrogio L, Lira SA, Raine CS. Neuroprotection and remyelination after autoimmune demyelination in mice that inducibly overexpress CXCL1. Am J Pathol, 2009, 174:164-176
Note: If no author is given, the source is cited instead.
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