The very inflammatory mechanism that causes the demyelination at the root of MS could serve as a radical new means to fight the illness, according to a new study ahead of print in the Journal of Clinical Investigation.

Researchers at Israel's Weizmann Institute of Science used mice and rats to model the symptoms of MS.  They examined the mice's brains with special attention to special immune cells called microglia that have been implicated in the uncontrolled inflammation that characterizes MS.

When microglias are exposed to high doses of a pro-inflammatory protein known as IFN-gamma, they produce another protein known as tumor necrosis factor-alpha (TNF-alpha).  This production of TNF-alpha is considered an important cause of demyelination and loss of nerve function in patients with MS.

The researchers found, however, that exposing the microglias to small amounts of IFN-gamma or an anti-inflammatory protein known as IL-4, both produced by immune cells known as helper T cells, could actually stimulate the microglias to support nerve cell survival, rather than destruction.

Based on the study's findings, the authors suggested "that rather than suppression, immunomodulation aimed at appropriate and well-controlled activation of microglias might be the approach to adopt in designing ways to promote cell renewal under neurodegenerative conditions."

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