Department of Ophthalmology, Changzheng Hospital of Naval Medicine University, Shanghai, China.
Front Immunol. 2024 May 16;15:1392956. doi: 10.3389/fimmu.2024.1392956. eCollection 2024.
Thyroid eye disease (TED) is a disfiguring autoimmune disease characterized by changes in the orbital tissues and is caused by abnormal thyroid function or thyroid-related antibodies. It is the ocular manifestation of Graves' disease. The expression of thyroid-stimulating hormone receptor (TSHR) and the insulin-like growth factor-1 receptor (IGF-1 R) on the cell membrane of orbital fibroblasts (OFs) is responsible for TED pathology. Excessive inflammation is caused when these receptors in the orbit are stimulated by autoantibodies. CD34 fibrocytes, found in the peripheral blood and orbital tissues of patients with TED, express immune checkpoints (ICs) like MHC II, B7, and PD-L1, indicating their potential role in presenting antigens and regulating the immune response in TED pathogenesis. Immune checkpoint inhibitors (ICIs) have significantly transformed cancer treatment. However, it can also lead to the occurrence of TED in some instances, suggesting the abnormality of ICs in TED. This review will examine the overall pathogenic mechanism linked to the immune cells of TED and then discuss the latest research findings on the immunomodulatory role of ICs in the development and pathogenesis of TED. This will offer fresh perspectives on the study of pathogenesis and the identification of potential therapeutic targets.
甲状腺眼病（TED）是一种以眼眶组织改变为特征的致盲性自身免疫性疾病，由甲状腺功能异常或甲状腺相关抗体引起，是格雷夫斯病的眼部表现。眼眶成纤维细胞（OFs）细胞膜上甲状腺刺激激素受体（TSHR）和胰岛素样生长因子-1 受体（IGF-1R）的表达是 TED 病理学的基础。当这些自身抗体刺激眼眶中的这些受体时，会引起过度炎症。在 TED 患者的外周血和眼眶组织中发现的 CD34 纤维母细胞表达免疫检查点（IC），如 MHC II、B7 和 PD-L1，这表明它们在 TED 发病机制中具有抗原呈递和调节免疫反应的潜在作用。免疫检查点抑制剂（ICIs）显著改变了癌症治疗方法。然而，在某些情况下，它也会导致 TED 的发生，这表明 TED 中存在 IC 异常。这篇综述将全面探讨与 TED 免疫细胞相关的发病机制，然后讨论 IC 在 TED 发生和发病机制中的免疫调节作用的最新研究发现。这将为研究发病机制和确定潜在的治疗靶点提供新的视角。
