( king the actions of a hormone called IG...)UCLA study uncovers clues for why Graves' disease attacks the eyes

king the actions of a hormone called IGF-1, or insulin-like growth factor 1. Similar to insulin, IGF-1 stimulates cell growth while suppressing normal cell death. The team suspects that this mechanism prolongs the survival of older T-cells, causing a cascade of autoimmune problems that spur the body to attack its own tissue.

"We think that the extra receptors allow the new antibody and IGF-1 to disrupt the programming of the T-cells," said 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.

"The antibody provokes the receptor to signal the T-cell to grow and multiply ?long after the cell was programmed to die," he explained. "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."

The next step is to identify what the T-cells are reacting to and how the receptor enables the cells to survive beyond their normal lifespan. The team plans to develop an antibody drug to block the receptor from interacting with the T-cells and slow down the disease.

In Graves?disease, the thyroid gland goes into overdrive, producing excess levels of hormone that attack the tissue behind the eye, causing them to protrude. In extreme cases, patients experience trouble closing their eyelids, severe double vision, corneal scarring, optic nerve damage and even blindness.

Graves?disease is nine times more common in women than men. The disorder most often strikes during the childbearing years, and runs an average course of one to two years. No cure exists, though surgery can be done at the end stage to correct disfigurement.
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Source:University of California - Los Angeles

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