A recent study has found supporting evidence to implicate insulin-like growth factor receptor (IGF-1R) in the development of Graves’ disease.//
In a previous research, Terry J. Smith, M.D. and Raymond Douglas, M.D., Ph.D. had identified the interaction between immunoglobulins and IGF-1R as a cause of inflammation and lymphocyte infiltration in both Graves’ disease and rheumatoid arthritis.
The discovery of these mechanisms in a similar class of autoimmune diseases supports the belief that a single biological mechanism is activating a variety of autoimmune diseases. The identification of such a mechanism may lead to a common therapeutic strategy for these conditions.
According to Dr. Smith, "We continue to build a body of evidence that suggests that a single biological mechanism can activate a variety of autoimmune diseases. It is possible that these findings will allow us for the first time to interrupt the disease process before any lasting damage is done. It could be involved in other autoimmune disorders as well; we're thinking about a large number of diseases."
In the article appearing in the March 1, 2007 issue of the Journal of Immunology, Dr. Smith and his colleagues report that a disproportionately large fraction of peripheral blood T cells express IGF-1R in patients with Graves’ disease. The results support a potential role for IGF-1R as a determinant of immune responses through fibroblast and lymphocyte activation and expansion. This further implicates IGF-1R in the pathogenesis of patients with Graves’ disease.
Graves' disease, the most common cause of hyperthyroidism, can lead to severe swelling around the eye sockets. It 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 in the same class include rheumatoid arthritis, multiple sclerosis, and lupus. 37,000 new Page: 1 2 Related medicine news :1
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