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 SAN DIEGO, March 4 /PRNewswire/ -- Scientists at Stanford University and Neurocrine Biosciences Inc., a San Diego-based biopharmaceutical company, have discovered the dominant immune response which causes multiple sclerosis (MS). The research, reported in the March 4 issue of Nature, has identified the rogue immune cells that are responsible for the aberrant auto-immune response indicative of the disease. The results of the research could lead to therapies and possibly a cure for the disease which afflicts 250,000 to 350,000 people in the United States alone, according to Gary A. Lyons, president and chief executive officer.
 "Scientists have known that MS was an auto-immune disease and for 20 years have been trying to identify which immune cells cause the immune response," Lyons said. "Dr. Lawrence Steinman and his team have identified the specific T-lymphocytes that attack a fragment of the myelin basic protein (MBP), a component of the myelin sheath that surrounds nerve fibers. Now we can turn our focus towards developing a therapeutic which destroys the cells, provoking the autoimmune response without suppressing the patient's immune system."
 Typically afflicting people between 20 and 40 years of age, multiple sclerosis is a neurological disease in which the body's own immune system attacks the central nervous system. Specifically, the body's T-lymphocytes attack segments of the myelin sheath, the insulation material that surrounds nerve fibers. This results in scarring around nerve fibers, often leading to progressive paralysis. There seems to be a genetic predisposition to the disease, with more than twice as many women afflicted as men, but the biological mechanisms that trigger the disease are not clearly understood.
 As reported in Nature, researchers at Stanford University, led by Professor of Neurology Lawrence Steinman, M.D., analyzed T-cell receptor (TCR) genes taken directly from the MS brain plaques of 16 patients. Analysis of the gene sequences showed that a specific sequence was common to eight of the patients. Surprisingly, it was the identical gene sequence that causes the immune response in the animal model for MS. Researchers then worked to match this gene sequence with the known MBP gene sequence. In short, researchers had found the "lock" on the myelin sheath and were looking for the matching "key" on the T-cell. Once the T-cell is activated and its "key" fits into the "lock" on the myelin sheath, the MS disease process begins.
 "We identified the TCR gene sequence that bound to the common MBP fragment found in MS patients," Steinman said. "By knowing this sequence we can now proceed to develop therapeutics to combat the disease."
 Neurocrine Biosciences has an exclusive license for this technology which was developed at Stanford. Neurocrine has already begun developing a protein-based therapy that can cross the blood- brain barrier and interfere with the T-cells' ability to bind to the MBP segment, thereby halting the disease. The work will be performed under the direction of Steinman, who is Neurocrine's chief scientist/immunology.
 "This is the most practical approach with the shortest development time before proceeding to clinical trials," Steinman added. "We will also be pursuing the development of small molecules that will either remove or inactivate these T-cells from the body and possibly begin work on a vaccine that will disable the specific T- cells that initiate the attack. All three methods focus on blocking or disabling the very specific immune response that causes this disease, without suppressing the patient's entire immune system."
 While this research identifies the specific autoimmune response that causes the disease, researchers still do not understand what triggers the T-cell to attack.
 "A probable answer could be the notion of molecular mimicry,' whereby this fragment of myelin resembles fragments of common viral pathogens like influenza or measles," Dr. Steinman said. "Infection by this pathogen may trigger autoimmunity, with T-cells attacking the viral pathogen and at the same time attacking the myelin fragment that has a similar structure. Recent work in our lab and Dr. Hugh McDevitt's lab at Stanford indicates that the amino acid sequence of a virus need only be identical for five amino acids within a stretch of 10 amino acids of MBP in order to trick the T-cell into an autoimmune response."
 Neurocrine Biosciences Inc. was organized in January 1992, to develop novel pharmaceutical products to treat diseases resulting in aging- and stress-related disregulation of the nervous, immune and endocrine systems. The company has raised initial capital financing from Avalon Medical Partners, D. Blech & Co., and Kleiner Perkins Caufield and Byers.
 -0- 3/4/93
 /CONTACT: Kevin C. Gorman, Ph.D., director of corporate development, 619-454-3803, or Lawrence Steinman, M.D., chief scientist/Immunology, 415-725-6401, both of Neurocrine Biosciences; or Linda Seaton of Keatinge/Seaton Communications, 619-625-2100, for Neurocrine Biosciences/

CO: Neurocrine Biosciences Inc.; Stanford University ST: California IN: MTC SU:

MS-JB -- SD002 -- 2832 03/04/93 09:16 EST
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Publication:PR Newswire
Date:Mar 4, 1993

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