关键词: Hashimoto thyroiditis electron microscopy myofibroblasts ultrastructure

来  源:   DOI:10.4183/aeb.2023.415   PDF(Pubmed)

Abstract:
UNASSIGNED: 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.
UNASSIGNED: Our ultrastructural study aims to delineate the presence and contribution of MFBs to the fibrotic milieu of HT.
UNASSIGNED: Tissue biopsies were obtained from 5 HT-diagnosed patients and specimens were examined using a Transmission Electron Microscope (TEM).
UNASSIGNED: 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).
UNASSIGNED: 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.
摘要:
桥本甲状腺炎(HT)是一种与甲状腺功能减退相关的自身免疫性疾病。导致甲状腺滤泡细胞破坏的淋巴细胞浸润被胶原蛋白产生的增加所抵消。沉积和疤痕。然而,直到最近,具有收缩特性的修饰成纤维细胞的特定亚群,即“肌成纤维细胞”(MFBs)与HT相关。
我们的超微结构研究旨在描绘MFBs对HT纤维化环境的存在和贡献。
从5名HT诊断的患者获得组织活检,并使用透射电子显微镜(TEM)检查样本。
组织病理学检查显示HT样本中甲状腺滤泡细胞的广泛微绒毛萎缩和非典型空泡形成。除了间质外渗的淋巴细胞,毛细血管被具有特征性电子致密α-平滑肌肌动蛋白(α-SMA)的MFBs(与管腔的平均距离为1.248±0.43µm)包围,可以在更高的放大倍数中确认。与受损的内皮衬里相比,发现肌纤维母细胞突起在毛细血管腔附近具有明显更高的代表性(P<0.01)。
我们的TEM研究结果表明,肌纤维母细胞突起对内皮的侵入可能是导致HT患者卵泡细胞功能异常的一个重要因素,并提供了对可能是HT病理基础的超微结构相互作用的典型理解。
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