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Natural immune response reduces nerve damage; may lead to improved treatment for spinal cord injury

In a series of animal experiments, scientists show for the first time that damage to the central nervous system causes the body to mount an immune reaction against itself that actually protects neurons from further damage. The findings may lead to a vaccine to improve functional recovery following spinal cord injury.

The findings also challenge accepted dogma that immune activity in the central nervous system is harmful, and that immune response against the bodys own tissue, known as an autoimmune response, is destructive. We show that this autoimmune response can help the individual to cope with stress caused by the injury, says lead author Michal Schwartz, PhD, of the Weizmann Institute of Science in Rehovot, Israel. The study, funded in part by Proneuron, Ltd., an Israeli biotechnology company, appears in the June 1 issue of The Journal of Neuroscience. Schwartz has an equity position in Proneuron.

These studies provide new avenues for development of potential treatments and prevention of paralysis resulting from injury, says Esther Sternberg, MD, an expert on the interaction of the nervous system and immune system at the National Institute of Mental Health in Bethesda, MD.

The potential treatment could boost in a well-controlled way the natural protective autoimmune response, and thereby inhibit the cascade of normal damage that occurs after the initial trauma, such as spinal cord injury.

In four experiments in rats and mice, Schwarz and colleagues Eti Yoles and Ehud Hauben found that central nervous system trauma evokes a protective immune response that reduces neuronal loss.

The authors say that the ability to spontaneously mount a protective immune response does not exist in all individuals, but can be induced in deficient individuals or boosted if it exists. Since this response represents the bodys own attempt to heal itself, stimulating or boosting it is likely to provide the most comprehensive protection for damaged nerves.


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Contact: Mary McComb
mary@sfn.org
202-462-6688
Society for Neuroscience
28-May-2001


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