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Does autoimmunity against thyroglobulin play a role in the pathogenesis of Graves’ ophthalmopathy: a review

Authors Shanmuganathan T, Girgis C, Lahooti H, Champion B, Wall J

Received 12 May 2015

Accepted for publication 11 July 2015

Published 3 December 2015 Volume 2015:9 Pages 2271—2276

DOI https://doi.org/10.2147/OPTH.S88444

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Yang Liu

Peer reviewer comments 2

Editor who approved publication: Dr Scott Fraser


Thayalini Shanmuganathan,1 Christian Girgis,2 Hooshang Lahooti,1 Bernard Champion,1 Jack R Wall1

1Department of Medicine, Nepean Clinical School, Nepean Hospital, The University of Sydney, Sydney, 2Department of Medicine, Westmead Millennium Institute, The University of Sydney, Sydney, NSW, Australia

Abstract: While most authors believe that autoimmunity against the TSH receptor expressed in the orbital connective tissue cells is the main reaction that leads to the development of ophthalmopathy in patients with Graves’ hyperthyroidism, an older hypothesis that deserves fresh consideration is based on the notion that thyroglobulin (Tg) in the thyroid gland passes in a retrograde fashion to the orbit where it is recognized by Tg autoantibodies, leading to inflammation. Here, we review new evidence that supports a role of Tg and propose a new hypothesis based on the notion that Tg is targeted in the orbit leading to a complex cascade of reactions that leads to Graves’ ophthalmopathy.

Keywords: ophthalmopathy, Graves’ disease, thyroglobulin, thyroid peroxidase, TSH receptor, lymphocytes, autoantibodies
 

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