Immunopathogenesis of Graves' ophthalmopathy: the role of the TSH receptor.
Immunopathogenesis of Graves' ophthalmopathy: the role of the TSH receptor.
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DOI：
10.1016/j.beem.2011.10.003
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发表时间：
2012-06
期刊：
影响因子：
--
通讯作者：
Bahn R
中科院分区：
文献类型：
--
作者：
Iyer S;Bahn R
Graves眼病是一种眼眶炎性自身免疫性疾病。Graves'甲亢和眼病之间的密切临床和时间关系长期以来一直表明，这两种情况来自一个单一的全身过程，并共享促甲状腺激素受体作为一个共同的自身抗原。这种受体不仅在甲状腺滤泡细胞中表达，而且在眼眶成纤维细胞中表达，在眼病患者的眼眶细胞中测得的水平高于正常个体的细胞。最近几个实验室的研究表明，眼眶成纤维细胞中的促甲状腺激素受体激活可增强透明质酸合成和脂肪生成，这两种细胞功能似乎在患病眼眶中上调。磷酸肌醇3-激酶/Akt信号级联，沿着其他效应途径，包括腺苷酸环化酶/cAMP，似乎介导这些过程。这种情况的未来疗法可能涉及抑制眼眶成纤维细胞中的促甲状腺激素受体信号。
Graves’ ophthalmopathy is an inflammatory autoimmune disorder of the orbit. The close clinical and temporal relationships between Graves’ hyperthyroidism and ophthalmopathy have long suggested that both conditions derive from a single systemic process and share the thyrotropin receptor as a common autoantigen. This receptor is expressed not only in thyroid follicular cells, but also in orbital fibroblasts with higher levels measured in orbital cells from ophthalmopathy patients than in cells from normal individuals. Recent studies from several laboratories have shown that thyrotropin receptor activation in orbital fibroblasts enhances hyaluronic acid synthesis and adipogenesis, both cellular functions that appear to be upregulated in the diseased orbit. The phosphoinositide 3-kinase/Akt signaling cascade, along with other effector pathways including adenylyl cyclase/cAMP, appears to mediate these processes. Future therapies for this condition may involve inhibition of thyrotropin receptor signaling in orbital fibroblasts.
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