Blocking immune response to spinal cord injury can improve chances for recovery

Irvine, Calif., Nov. 13, 2003 -- People who suffer spinal cord injuries may have a greater chance of recovery if treated with drugs that block the body's own immune response to the initial trauma, researchers from the Reeve-Irvine Research Center at UC Irvine have found. In addition, UCI neurologist Hans Keirstead and immunologist Thomas Lane have laid the foundation for these drugs by creating antibodies that, when tested on rats, stopped the secondary nerve and spinal cord damage caused by the immune system response. Use of these antibodies resulted in significantly improved rates of recovery.

Previous studies have shown that the body's immediate immune system response to a spinal cord injury actually worsens the condition. Results of this UCI study appear in the November issue of Experimental Neurology.

"While the primary tissue damage caused by the initial spinal trauma cannot be reversed, we've discovered that the secondary damage caused by immune responses can be prevented, which gives those who suffer these injuries hope for recovery," Keirstead said.

Immediately after spinal cord trauma, cells called chemokines are released at the injury site and induce inflammation. One specific chemokine called CXCL-10 recruits immune system cells called T-lymphocytes. Normally, T-cells battle disease and other invading agents in the body, but in the central nervous system during spinal injury and periods of disease in multiple sclerosis, these T-cells create toxic compounds that attack and damage spinal tissue and nerve fibers.

In tests on rats with induced spinal cord injuries, Keirstead and Lane treated one group with their antibody drugs that blocked CXCL-10 cells from recruiting T-cells to the injury site. Another group received no therapies. In the group treated with the antibodies, the researchers found a significant reduction in T-cell counts and spinal damage. The untreated rats showed increased T-cell levels and greater secondary tissue d

Contact: Tom Vasich
University of California - Irvine

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