Study Finds Clues to Graves' Disease Assault on Eyes

Thyroid disorder disrupts T-cell programming, sparking body to attack its own tissue

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FRIDAY, March 2, 2007 (HealthDay News) -- Researchers at the University of California, Los Angeles have found new clues about what causes Graves' disease, an autoimmune disorder that involves overactivity of the thyroid gland.

The findings may provide a new target to treat the disease, which can damage the tissue behind the eyes and cause them to bulge painfully from their sockets. In extreme cases, patients can suffer severe double vision, corneal scarring, optic nerve damage, and even blindness.

The UCLA team identified defects in the infection-fighting T-cells of immune systems in people with Graves' disease. The study was published March 1 in the Journal of Immunology.

Previous research found that the immune systems of patients with the disease produce an antibody that attacks the thyroid, causing inflammation and damage to the body, including eye tissue. Healthy people do not produce this antibody.

In the new study, the UCLA researchers examined T-cells from Graves' disease patients and found that the cells contain an abnormal surplus of the receptor targeted by the previously identified antibody. The scientists believe the antibody latches onto these receptors and disrupts the programming of the T-cells, which triggers a sequence of events that causes the immune system to attack its own tissue.

"The antibody provokes the receptor to signal the T-cell to grow and multiply -- long after the cell was programmed to die," principal investigator Dr. Terry Smith, professor of medicine at the David Geffen School of Medicine and chief of molecular medicine at Harbor-UCLA Medical Center, said in a prepared statement.

"After two or three generations of this process, we suspect that the high-jacked T-cells mutiny over the normal T-cells, sparking the body's immune reaction against itself," Smith said.

More information

The U.S. National Library of Medicine has more about Graves' disease.

SOURCE: University of California, Los Angeles, news release, March 1, 2007

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