Journal
SURVEY OF OPHTHALMOLOGY
Volume 55, Issue 3, Pages 215-226Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.survophthal.2009.06.009
Keywords
Graves ophthalmopathy; immunology; orbit; thyroid eye disease
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Funding
- NEI NIH HHS [K23 EY016339, K23 EY016339-02] Funding Source: Medline
- NIDDK NIH HHS [R01 DK063121] Funding Source: Medline
- NATIONAL EYE INSTITUTE [K23EY016339] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK063121] Funding Source: NIH RePORTER
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Graves disease represents a systemic autoimmune process targeting the thyroid, orbit, and pretibial skin. The thyroid dysfunction is treatable, but no consistently effective medical therapy has yet been described for the orbital manifestations of Graves disease, also known as thyroid-associated ophthalmopathy or thyroid eye disease. Several autoantigens are potentially relevant to the pathogenesis of thyroid eye disease. Activating antibodies generated against the thyrotropin receptor can be detected in a majority of patients, and these drive hyperthyroidism. However, stimulating antibodies against the insulin-like growth factor-1 receptor (IGF-IR) may also play a role in the extra-thyroid manifestations of Graves disease. IGF-IR is overexpressed by orbital fibroblasts derived from patients with thyroid eye disease, whereas IGF-IR+ T and IGF-IR+ B cells are considerably more frequent in Graves disease. Actions of several cytokines and the molecular interplay peculiar to the orbit appear to provoke the inflammation, fat expansion, and deposition of excessive extracellular matrix molecules in thyroid eye disease. Based upon these new insights, several therapeutic strategies can now be proposed that, for the first time, might specifically interrupt its pathogenesis. (Surv Ophthalmol 55:215-226, 2010. (C) 2010 Elsevier Inc. All rights reserved.)
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