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Selectively blocking inflammatory signals may protect mice from MS

ut of 20 mice with both high interferon levels and the SOCS1 gene had symptoms.

On autopsy, mice with high interferon levels in the nervous system had severe loss of oligodendrocytes, ranging from 20 to 40 percent. Those with the protective SOCS1 gene lost only eight to 15 percent.

High interferon levels were also associated with loss of myelin sheaths around nerve connections and unprotected axons in the brain. Again, SOCS1 was able to reduce the damage.

"Together," the researchers wrote, "these data demonstrate that oligodendroglial expression of SOCS1 protects mice from the clinical and morphological consequences of IFN-gamma expression in the central nervous system during development."

"We found this tremendously encouraging," said Popko. "SOCS1 prevented or reduced the harmful effects of interferon gamma on myelin-producing cells. This study solidifies our suspicions about interferon's specific role in demyelinating disease and suggests ways to block it."

Although there is currently no reliable way to deliver SOCS1 directly to the nerves of a patient with multiple sclerosis, this protective approach could be combined with stem cell therapy to repair nerve damage. Several research groups are already studying the use of stem cells to repair damaged myelin sheaths, but in the long term those stem cells would be vulnerable to ongoing immune-mediated damage.

But if stem cells could be engineered to resist harmful signals such as interferon-gamma, they might be protected from the "harsh environment" present in immune mediated demyelinated lesions, said Popko.


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Source:University of Chicago Medical Center


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