眼眶成纤维细胞在内分泌性眼病中的形态功能特征及免疫调节

E. S. Taskina, S. V. Kharintseva
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引用次数: 3

摘要

内分泌性眼病(EOP)是一种慢性疾病,以甲状腺功能障碍患者球后软组织进行性自身免疫性炎症为特征。眼眶成纤维细胞以其独特的形态功能特性在眼外肌和/或球后组织的浸润过程和纤维化的发病机制中起着重要的作用。与其他定位成纤维细胞不同,它们不是起源于中胚层,而是起源于神经外胚层。这篇综述了解了这些细胞在疾病的不同活动阶段的调节的免疫学方面。细胞间与t淋巴细胞(CD40-CD154)的相互作用导致眼眶成纤维细胞活化,促甲状腺激素病理受体的表达增加,细胞间基质成分、粘附分子、生长因子、细胞因子和前列腺素的产生。本文给出了眼眶成纤维细胞亚群的详细形态功能特征和调节其转分化为脂肪细胞和肌成纤维细胞的机制。本文分析了t -辅助型17对眼眶成纤维细胞Thy1+/Thy1- (CD90+/CD90-)功能活性的影响。进一步研究眼窝成纤维细胞在EOP中的特征及其与各种免疫细胞的细胞间相互作用具有重要意义,这可能有助于揭示这种病理的新发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Morphofunctional characteristics and immunological regulation of the orbital fibroblasts function in endocrine ophthalmopathy
Endocrine ophthalmopathy (EOP) is a chronic disease characterized by progressive autoimmune inflammation of the soft retrobulbar tissues in thyroid dysfunction. The orbital fibroblasts with their unique morphofunctional properties are very important in the pathogenesis of the infiltrative process and fibrosis of the extraocular muscles and/or retrobulbar tissue. They, unlike other localization fibroblasts, have not mesodermal, but neuro-ectodermal origin. The review acquaints with the immunological aspects of the regulation of these cells in different activity phases of disease. Intercellular interaction with T-lymphocytes (CD40-CD154) leads to orbital fibroblasts activation with increased expression of pathological receptors for thyroid-stimulating hormone, as well as production of intercellular matrix components, adhesion molecules, growth factors, cytokines and prostaglandins. Detailed morphofunctional characteristics of the orbit fibroblast subpopulations and mechanisms regulating their transdifferentiation into adipocytes and myofibroblasts are given. The analysis of literature data on the effect of T-helper type 17 on the functional activity of Thy1+/Thy1- (CD90+/CD90-) orbital fibroblasts is presented. The importance of the further study of the orbital fibroblasts characteristics in EOP and their intercellular interaction with various immune cells was noted, which may be able to uncover new pathogenetic mechanisms of this pathology.
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