TSH Receptor and IGF1 Receptor Expression in Circulating Fibrocytes in the Pathogenesis of Graves’ Orbitopathy
crossref（2024）
Institute of Post Graduate Medical Education and Research and SSKM Hospital
Abstract
Purpose Graves’ Orbitopathy (GO), an autoimmune disorder linked to Graves’ Disease (GD), manifests through inflammation in orbital tissues and extraocular muscles (EOMs), driven by key receptors like TSHR and IGF1R. It was observed that a certain individual with GD will develop clinically significant orbitopathy and reason behind this still unclear. This study aimed to elucidate this connection by: i) Assessing IGF1R expression and its correlation with TSHR on circulating fibrocytes. ii) Investigating fibrocyte conversion to fibroblasts upon serum treatment. iii) Analysing cytokine and chemokine expression in fibrocytes post-serum exposure within the Indian population. Methods and Results Flow cytometry analysis of IGF1R in peripheral blood from 30 GO, 30 GD, and 20 healthy controls (HC) revealed significantly elevated IGF1R+ fibrocytes in GO (11%) versus GD (2.4%) and HC (0.1%). Immunocytochemistry of TSHR and IGF1R on cultured fibrocytes confirmed colocalization of TSHR and IGF1R on fibrocytes, notably higher in GO. Treating HC-derived fibrocytes with GO patient serum triggered fibroblast transformation, marked by increased fibrotic markers (CD90, alpha SMA). Moreover, sandwich ELISA of cytokines and chemokines like IL-6, IL-8, TNF-α, MCP-1, and HA demonstrated elevated levels of those cytokines and chemokines in GO serum-treated HC-fibrocytes. Conclusion These results highlight the potential pathogenicity of TSHR and IGF1R on fibrocytes in GO, suggesting their role in orbital tissue remodelling and inflammation. The observed receptor colocalization may drive GO pathogenesis, providing insights into targeted therapeutic strategies for this debilitating condition.
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