ArticleFrontiers in endocrinology2020
Immunological Features of Paranasal Sinus Mucosa in Patients with Graves' Orbitopathy.
Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Contiguous orbital inflammation from paranasal sinus abnormalities in etiology of thyroid-associated ophthalmopathy.International journal of ophthalmology · 2026Article
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- Weak acid-initiated slow release of Dexamethasone from hydrogel to treat orbital inflammation.Theranostics · 2023Article
- Disulfiram Exerts Antifibrotic and Anti-Inflammatory Therapeutic Effects on Perimysial Orbital Fibroblasts in Graves' Orbitopathy.International journal of molecular sciences · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Previous studies showed that patients with Graves' orbitopathy (GO) had concomitant mucosal abnormality within the paranasal sinuses. It remains unknown whether the immunological reactions in sinus mucosa affect the orbit inflammation in GO. Methods: Patients with GO underwent sinus computed tomography (CT) scans for sinus mucosal disease by two independent reviewers using the Lund-MacKay systems. Ethmoid mucosal samples were collected during orbital decompression surgeries for patients with GO and correction surgeries for patients with old orbital fractures as controls. Histological analysis and immunofluorescence were performed in all sinus mucosa tissues. Flow cytometry analysis was used to examine the immunological features of sinus mucosa in both GO and control groups. Results: Immunohistochemistry showed that the paranasal sinus mucosa of patients with GO grew swelling, with goblet cell and small vessel proliferation, endothelial cell swelling, and inflammatory cell infiltration. The number of T helper (Th)1, Th17, and gamma-delta T cells in nasal sinus mucosa of patients with GO increased significantly compared with those from controls. Further, the proportion of Th1 cells was significantly correlated with clinical activity score. In addition, there was a decreased number of regulatory T cells in patients with GO. The number of Th2 cells showed no significant difference between the two groups. Finally, the proportion of interleukin-22-producing cell subsets in gamma-delta T cells of patients with GO was significantly increased compared with those from controls. Conclusions: Our observations illustrated a potential pathogenic role of mucosal-infiltrating T cells, which may have the possibility to aggravate inflammatory responses in GO.
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