More MS news articles for December 1999

UAB researchers develop new model to combat Multiple Sclerosis

The University of Alabama at Birmingham Office of Media Relations

December 6, 1999
Contact: Bob Shepard
205-934-8934
bshep@uab.edu

BIRMINGHAM, Ala., -- Researchers at UAB (University of Alabama at Birmingham) have shown that by manipulating the immune system they can prevent or slow the progression of multiple sclerosis (MS) in mice. The findings, published in this month's issue of the Journal of Immunology, may have positive implications for the 300,000 Americans with MS. The research focuses on a part of the immune system known as the complement system.

In a normal, healthy immune system, proteins that make up the complement system are activated to fight back whenever the body is invaded by an outside bacteria or virus. Half of all complement proteins are called activators, which fight an invader. The other half are regulators, which control the complement activation and shut it off when the battle is over. If uncontrolled, activators have been shown to cause severe inflammation and tissue destruction.

"In autoimmune diseases such as multiple sclerosis, the body attacks itself in a confused immune response," says Scott Barnum, Ph.D., assistant professor of microbiology and the senior author of the report. "Complement activators become a large part of that attacking force, causing inflammation and destruction of certain brain cells that protect nerves. The regulator proteins are overwhelmed, and are not able to control the activators."

Working in mice, Barnum succeeded in altering a regulator complement protein called CRRY so that it was produced in and continually present within the brain. When the mouse's complement system was activated in the presence of the animal form of MS, the CRRY regulator was already on hand to shut down the activators and reduce inflammation and tissue damage.

"All of the animals in our study that carried the CRRY protein either did not get MS or had very delayed onset of symptoms," says Barnum.

While complement proteins have been implicated in causing inflammation in central nervous system disease in the past, this is the first research that indicates manipulating the complement system might be a therapeutic method to treat MS. Manipulation of CRRY may also play a role in treating other autoimmune diseases or central nervous system conditions such as traumatic brain injury or stroke, making this model useful for examining many chronic inflammatory conditions.

www.uab.edu/news