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Protein pieces halt autoimmune response.

In the disease known as myasthenia gravis, the immune system attacks regions where nerve and muscle meet, causing fatigue and loss of muscle control. At these junctions, a nerve ending normally sends chemical signals across a gap to stimulate muscle contraction. But in myasthenia gravis, antibodies destroy the muscle's receptor proteins that serve as docks for this signal, a chemical called acetylcholine.

Immune-system cells called T-cells play a key role in this autoimmune response. They break down acetylcholine-receptor proteins, creating two short fragments easily recognized by the immune system. The fragments then cause other immune-system cells to proliferate and make the antibodies.

Synthetic protein fragments that differ from the receptor's fragments by just one amino acid can inhibit this proliferation, says Edna Mozes of the Weizmann Institute of Science in Rehovot, Israel. Inhibition occurs both in cultured cells and in laboratory mice, she and her co-workers report in the Aug. 1 Proceedings of the National Academy of Sciences.

It seems the T-cells do not distinguish between the synthetic fragments and the receptor's own pieces, so they readily link to the lab-made versions, notes Mozes. However, the synthetic fragments fail to initiate the rest of the destructive immune-system response.

The researchers also report that the two most potent artificial fragments have quelled up to 100 percent of the response of T-cells taken from people with myasthenia gravis. This leads them to hope that such fragments will point the way to an effective therapy.
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Publication:Science News
Article Type:Brief Article
Date:Aug 14, 1993
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