How a new eye medicine stops TED from making eyes bulge

Original Title

The therapeutic revolution in thyroid eye disease: from orbital radiotherapy to teprotumumab and AI

Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms

Summary

TED is when the tissue behind the eyes swells up and pushes them forward, often because the immune system gets confused and attacks the eyes. A new medicine called teprotumumab blocks a signal (IGF-1R) that makes this swelling happen.

Proposed Mechanism
TSHR-IGF-1R complex activation drives orbital fibroblast proliferation and glycosaminoglycan secretion
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IGF-1R signaling promotes orbital fibroblast adipogenesis via Thy-1-negative subpopulation activation
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IGF-1R signaling enhances T-cell survival and autoimmunity by inhibiting apoptosis via PI3K/Akt
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IGF-1R signaling enhances B-cell proliferation and autoantibody production
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TSHR activation upregulates miR-146a and miR-155 to promote fibroblast proliferation
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Epac1 deficiency promotes orbital fibrosis via JAK/STAT3 pathway
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Treg/Th17 imbalance permits autoimmune attack in TED
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Mesenchymal stem cells inhibit orbital adipogenesis via IGF-binding protein and FAK/PI3K/Akt suppression
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Rapamycin inhibits CD4+ cytotoxic T cells via mTORC1 blockade to reduce TED severity
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Teprotumumab inhibits IGF-1R to reduce orbital inflammation and fibrosis
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