![]() ![]() Involvement of the former probably transcends disease boundaries, while TSHR may not.Ĭopyright © 2012. In sum, based on current evidence, IGF-1R and TSHR can be thought of as "partners in crime". Moreover, fibrocytes infiltrate both the orbit and thyroid in GD. When ligated by TSH or M22, a TSHR-activating monoclonal antibody, fibrocytes produce extremely high levels of several cytokines and chemokines. Levels of TSHR on fibrocytes greatly exceed those found on orbital fibroblasts. Functional TSHR and IGF-1R have also been found on fibrocytes, CD34⁺ bone marrow-derived cells from the monocyte lineage. IGF-1R forms a complex with TSHR which is necessary for at least some of the non-canonical signaling observed following TSHR activation. In addition, activating IgGs capable of displacing IGF-1 from IGF-1R have also been detected in patients with these diseases. These abnormal patterns of IGF-1R display are also found in rheumatoid arthritis and carry functional consequences. Elevated levels of insulin-like growth factor-1 receptor (IGF-1R) have been found in orbital fibroblasts as well as B and T cells from patients with GD. ![]() Also uncertain is the participation of other cell surface receptors in the disease. Less well elucidated is what part the TSHR pathway might play in the development of GO. The role of the thyroid stimulating hormone receptor (TSHR) and activating antibodies directed against it in the hyperthyroidism of Graves' disease (GD) is firmly established. The etiology of Graves' orbitopathy (GO) remains enigmatic and thus controversy surrounds its pathogenesis.
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