To die or not to die
The thyroid gland regulates the metabolism by producing hormones that are necessary for normal growth and maturation. Hormones are released when thyrocyte cells in the thyroid are stimulated. A new study in the December issue of Nature Immunology (Vol. 1, No. 6, 01 Dec 2000) explains the very different symptoms of Graves' disease and Hashimoto's thyroiditis, both autoimmune diseases of the thyroid, by the finding that these cells react very differently to signals that trigger them to die. In Graves' disease, thyroid cells proliferate and produce too much hormone. Conversely, Hashimoto's thyroiditis ultimately leads to insufficient hormone because the autoimmune disease causes the thyrocytes to die.
Researchers from Rome, Italy, showed that, although in both diseases thyrocytes display a protein that can trigger thyrocyte "suicide", only in Hashimoto's thyroiditis are the thyrocytes destroyed. This is because in Hashimoto's thyroiditis, the immune milieu produces proteins (cytokines) that favor the production of internal killing proteins in the thyrocytes. In Graves' disease, however, the cytokines trigger internal shields that protect against cellular "suicide". This understanding of how underlying differences in the immune environment cause such different diseases could aid the development of therapies that target the cytokines produced by the immune cells in each disease.
A News & Views was written on this paper by Douglas R. Green of the La Jolla Institute for Allergy & Immunology In San Diego.
Ruggero De Maria
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(C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza
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