Does autoimmunity against thyroglobulin play a role in the pathogenesis of Graves' ophthalmopathy: a review.
Sydney, Australia. In Clin Ophthalmol, 2014
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.
Recent insights into the cell biology of thyroid angiofollicular units.
Brussels, Belgium. In Endocr Rev, 2013
From onset, goiters are morphologically and functionally heterogeneous due to the polyclonal nature of the cells, with nodules distributed around areas of quiescent AFUs containing globules of compact thyroglobulin (Tg) and surrounded by a hypotrophic microvasculature.
Human fibrocytes coexpress thyroglobulin and thyrotropin receptor.
Ann Arbor, United States. In Proc Natl Acad Sci U S A, 2012
Findings suggest that thyroglobulin (Tg) and thyroid-stimulating hormone receptor (TSHR) detected in orbital connective tissues in thyroid-associated ophthalmopathy (TAO) result from local fibrocyte biosynthetic activity.