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."
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
New Candidate to Prevent Inflammation
Dr. Sonia Oliani and colleagues at So Paulo State University have identified a potential new molecule that inhibits inflammation, receptor for formylated peptides-2 (FPR-2). These findings are presented in the January 2009 issue of The American Journal of Pathology.
Inflammation of the peritoneum is characterized by severe abdominal pain. This inflammation can be prevented by annexin A1, which inhibits the migration of inflammation-inducing white blood cells into the affected area.
In this study, Gastardelo et al examined the identities of the receptors responsible for the anti-inflammatory effects of annexin A1 in a mouse model of peritonitis. FPR family members had been previously shown to interact with annexin A1. Yet
|Contact: Angela Colmone|
American Journal of Pathology