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Abstract
The pathophysiology underlying Graves’ disease and its ocular manifestation, thyroid associated ophthalmopathy (TAO) is not completely understood. Characterization of the mononuclear cells driving the disease and the cytokines they produce has led to significant advances in our understanding of TAO. This in turn has resulted in the identification of potentially attractive drug targets. For instance, development of specific cytokine pathway inhibitors for use in other autoimmune diseases now presents an opportunity for their application in TAO. In this paper, the authors review the rationale for considering anti-cytokine therapy in TAO, evidence linking specific cytokines such as IL-6, TNF-α, and IL-17 pathways to TAO, and explore the potential of targeting these pathways for therapy.
Financial & competing interests disclosure
This work was supported in part by National Institutes of Health grants EY008976, EY011708, DK063121, Center for Vision grant EY007003 from the NEI, an unrestricted grant from Research to Prevent Blindness, and the Bell Charitable Foundation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Key issues
Cytokine signaling pathways are intimately involved in the pathogenesis of autoimmune diseases.
Current evidence links several cytokine pathways to Graves’ disease.
Cytokine-based therapy has shown promise in allied diseases such as rheumatoid arthritis, psoriasis and Crohn’s disease.
IL-6, TNF-α and IL-17 are of particular interest as therapeutic targets in TAO.