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Researchers Identify Novel Disease Mechanism Associated with Graves' Disease

Discovery Holds Promise for Halting Disease Process in Several Autoimmune Disorders

Friday June 6, 12:08 pm ET
Source: Research & Education Institute
Business Wire
Torrance, Calif.

Investigators at the Research & Education Institute (REI) at Harbor-UCLA Medical Center have identified a novel disease mechanism underlying Graves' disease that may open the door to new therapies for this and possibly other debilitating autoimmune disorders, including multiple sclerosis, rheumatoid arthritis, and lupus.

In an article appearing in the June 15 issue of the Journal of Immunology, principal investigator Terry J. Smith, M.D., describes research that for the first time identifies an interaction between immunoglobulins found in Graves' patients and the insulin-like growth factor receptor (IGF-1R) as a cause of inflammation and lymphocyte infiltration.

Dr. Smith and his colleagues found that specific IgGs "turn on" the IGF-1R much like IGF-1 itself is known to do. Once the receptor is "on" a number of molecular events occur, including the production of two very powerful factors known to trigger T lymphocytes and direct them to sites of inflammation. Until now, the basis for this type of inflammation has been a mystery.

In addition, the researchers found that blocking the interaction between the IgG and IGF-1R arrests the progression of molecular events leading to T cell activation.

According to Dr. Smith, "It is possible that these findings will allow us for the first time to interrupt the disease process before any lasting damage is done, including sight loss."

Graves' disease, which is the most common cause of hyperthyroidism, can also lead to severe swelling around the eye sockets, producing the classic eye protrusion associated with some of the most advanced cases.

Graves' disease is part of a class of autoimmune disorders in which cellular defense mechanisms mistakenly identify the body's own tissues as foreign and seek to destroy them. Other autoimmune disorders include such ailments as rheumatoid arthritis, multiple sclerosis, and lupus.

"Autoimmune diseases are among the most insidious and debilitating of human ailments," said REI President and CEO Kenneth P. Trevett, J.D. "Dr. Smith's research suggests that there could be a common therapeutic strategy for these conditions -- potentially a huge advance in science and medicine. We are working closely with Dr. Smith and his colleagues to facilitate this work and promote its transfer to the patient bedside."

The Research & Education Institute at Harbor-UCLA Medical Center is the largest independent, not-for-profit biomedical research institute in Los Angeles County. Affiliated with both the David Geffen School of Medicine at UCLA and the Harbor-UCLA Medical Center, the Institute has an annual budget of over $60 million and currently supports more than 1,000 research studies in areas such as cardiology, emerging infections, cancer, women's health, reproductive health, vaccine research, respiratory physiology, neonatology, molecular biology, and genetics. REI also plays a pivotal role in the training of young physician-scientists and scientists-to-be and is active in promoting the health and well-being of nearby communities through community service programs that meet a variety of important social and medical needs.

Media Advisory:

Terry J. Smith, M.D. is a principal investigator at the Research & Education Institute (REI); a Professor of Medicine, UCLA School of Medicine; and Chief of the Division of Molecular Medicine at Harbor-UCLA Medical Center.

To schedule an interview, please contact Chris Lewis, REI Communications Office, 310/215-0234; cell 310/963-8745

CITATION: Journal of Immunology, Vol. 171, 6348-6354, June 15, 2003; electronic release June 6, 2003; "Anti-IGF-1R IgGs activate fibroblasts in Graves' disease."

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