Graves disease is the result of the production of autoantibodies to the TSHR located on the surface of thyroid cells. These antibodies bind the TSHR and stimulate it to overproduce thyroid hormones, which results in hyperthyroidism. In the June 16 issue of the Journal of Clinical Investigation, Sandra McLachlan and her team report that studies in a new adenovirus-mediated animal model of Graves disease revealed that cleavage of the TSHR A subunit can induce or amplify the immune response to the TSHR to a greater extent than the intact TSHR molecule.
The data, increase our understanding as to why autoantibodies specifically arise to the TSHR, stimulate the thyroid, and result in Graves hyperthyroidism. However, the mechanisms responsible for TSHR cleavage will require further exploration.
AUTHOR CONTACT:
Sandra M. McLachlan
Cedars-Sinai Medical Center, Los Angeles, California, USA.
Phone: 310-423-7680
Fax: 310-423-0221
E-mail: mclachlans@cshs.org
View the PDF of this article at: http://www.jci.org/cgi/content/full/111/12/1897
Journal of Clinical Investigation