ArticleThe Journal of clinical endocrinology and metabolism2022
Teprotumumab Divergently Alters Fibrocyte Gene Expression: Implications for Thyroid-associated Ophthalmopathy.
Article in The Journal of clinical endocrinology and metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- IL-11 receptor is a novel target for drug development with pharmacological activity in fibro-inflammatory disease.Scientific reports · 2026Review
- Macrophage plasticity in thyroid eye disease: dual effects of inflammation and fibrosis.Frontiers in immunology · 2026Review
- Article
- Identification of key extracellular proteins as the potential biomarkers in thyroid eye disease.PloS one · 2025Article
- Advances of IGF-1R inhibitors in Graves' ophthalmopathy.International ophthalmology · 2024Review
- Fibrocyte Participation in Thyroid-Associated Ophthalmopathy Suggests New Approaches to Therapy.Ophthalmic plastic and reconstructive surgery · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
contextTeprotumumab, an IGF-I receptor (IGF-IR) inhibitor, is effective in thyroid-associated ophthalmopathy (TAO). The drug can modulate induction by TSH of IL-6 and IL-8 in CD34+ fibrocytes and their putative derivatives, CD34+ orbital fibroblasts (CD34+ OF). Fibrocytes express multiple thyroid autoantigens and cytokines implicated in TAO, which are downregulated by Slit2. Inflammation and disordered hyaluronan (HA) accumulation occur in TAO. Whether teprotumumab alters these processes directly in fibrocytes/CD34+ OF remains uncertain.
objectiveDetermine teprotumumab effects on expression/synthesis of several TAO-relevant molecules in fibrocytes and GD-OF. DESIGN/SETTING/
participantsPatients with TAO and healthy donors were recruited from an academic endocrine and oculoplastic practice.
main outcome measuresReal-time PCR, specific immunoassays.
resultsTeprotumumab attenuates basal and TSH-inducible autoimmune regulator protein, thyroglobulin, sodium iodide symporter, thyroperoxidase, IL-10, and B-cell activating factor levels in fibrocytes. It downregulates IL-23p19 expression/induction while enhancing IL-12p35, intracellular and secreted IL-1 receptor antagonists, and Slit2. These effects are mirrored by linsitinib. HA production is marginally enhanced by teprotumumab, the consequence of enhanced HAS2 expression.
conclusionTeprotumumab affects specific gene expression in fibrocytes and GD-OF in a target-specific, nonmonolithic manner, whereas IGF-IR control of these cells appears complex. The current results suggest that the drug may act on cytokine expression and HA production systemically and locally, within the TAO orbit. These findings extend our insights into the mechanisms through which IGF-IR inhibition might elicit clinical responses in TAO, including a potential role of Slit2 in attenuating inflammation and tissue remodeling.
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