MYOFIBROBLASTS HINDER RECOVERY OF HASHIMOTO THYROIDITIS IN THE ULTRASTRUCTURAL LEVEL.

Pub Date : 2023-10-01 Epub Date: 2024-06-24 DOI:10.4183/aeb.2023.415
P Theotokis, A Gkantaras, E Avramidou, S Meditskou, M E Manthou
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Abstract

Background: Hashimoto thyroiditis (HT) is an autoimmune disorder associated with hypothyroidism. Lymphocyte infiltration leading to thyroid follicular cell destruction is counteracted by increased collagen production, deposition and scarring. However, only recently a specific subpopulation of modified fibroblasts with contractile properties, namely "myofibroblasts" (MFBs) have been linked to HT.

Aim: Our ultrastructural study aims to delineate the presence and contribution of MFBs to the fibrotic milieu of HT.

Material and methods: Tissue biopsies were obtained from 5 HT-diagnosed patients and specimens were examined using a Transmission Electron Microscope (TEM).

Results: Histopathological examination indicated extensive microvilli atrophy and atypical vacuolations of the thyroid follicular cells in the HT samples. In addition to interstitial extravasated lymphocytes, capillaries were encircled by MFBs (mean distance from lumen 1.248± 0.43µm) with the characteristic electron-dense α-smooth muscle actin (α-SMA), confirmable in higher magnifications. Myofibroblastic projections were found to have significantly higher representation near the capillary lumen compared to the impaired endothelial lining (P < 0.01).

Conclusion: Our TEM findings suggest that the intrusion of endothelia by myofibroblastic projections can be a significant factor towards the malfunction of follicular cells in HT patients and offer a paradigmal understanding of the ultrastructural interactions that may underlie the HT pathology.

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在超微结构层面,肌成纤维细胞阻碍了桥本氏甲状腺炎的康复。
背景:桥本甲状腺炎(HT)是一种与甲状腺功能减退症相关的自身免疫性疾病。淋巴细胞浸润导致甲状腺滤泡细胞破坏,而胶原蛋白生成、沉积和瘢痕形成的增加则抵消了淋巴细胞浸润。目的:我们的超微结构研究旨在确定甲状腺囊肿纤维化环境中是否存在甲状腺囊肿纤维母细胞,以及甲状腺囊肿纤维母细胞对甲状腺囊肿纤维化环境的贡献:组织活检取自 5 名确诊为 HT 的患者,使用透射电子显微镜(TEM)对标本进行检查:组织病理学检查显示,HT样本中的甲状腺滤泡细胞出现了广泛的微绒毛萎缩和非典型空泡。除了间质外渗淋巴细胞外,毛细血管还被MFB(与管腔的平均距离为1.248± 0.43µm)包围,MFB上有特征性的电子致密α-平滑肌肌动蛋白(α-SMA),在高倍放大镜下可以确认。与受损的内皮衬里相比,肌成纤维细胞突起在毛细血管腔附近的代表性明显更高(P < 0.01):我们的 TEM 研究结果表明,肌成纤维细胞突起对内皮的侵袭可能是导致 HT 患者卵泡细胞功能失常的一个重要因素,并提供了对可能导致 HT 病理的超微结构相互作用的范式理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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