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. 2022 Oct 22;43(4):1437–1449. doi: 10.1007/s10792-022-02537-6

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Graves Ophthalmopathy pathogenesis. Autoreactive T cells interact with orbital fibroblasts (OFs) via CD40:CD154 ligation. B cells differentiate into plasma cells, which synthesize and secrete TRAb. TRAb can mediate the autoimmune response of GO by recognizing TSHR. Activated OFs then secrete various inflammatory cytokines. TSHR and IGF-1R are expressed in the common area of the OFs membrane and exist in the form of a complex which plays a synergistic role in the functional regulation of orbital fibroblasts. Activated OFs can differentiate into either myofibroblasts or adipocytes and promote hyaluronan synthesis. As a result, orbital soft tissue expansion and congestion in GO. Created with BioRender.com