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淀粉样变苔藓。超微结构与发病机制。

Lichen amyloidosus. Ultrastructure and pathogenesis.

作者信息

Jambrosic J, From L, Hanna W

出版信息

Am J Dermatopathol. 1984 Apr;6(2):151-8. doi: 10.1097/00000372-198404000-00006.

DOI:10.1097/00000372-198404000-00006
PMID:6203424
Abstract

The ultrastructure of six cases of lichen amyloidosus was studied with special attention to epidermal keratinocytes and the role of tonofilaments as precursors of fibrils of amyloid. Through the process of apoptosis, keratinocytes undergo degeneration and become filamentous cells and then filamentous masses or Civatte bodies. These bodies then drop into the dermis through a damaged basement membrane. In the papillary dermis, islands of amyloid become closely associated with Civatte bodies. In some cases, conversion to straight nonbranching filaments, characteristic of fibrils of amyloid, was found within whorled, densely packed filamentous masses. The transformation into fibrils of amyloid was not observed in keratinocytes or Civatte bodies situated in the epidermis. This final step of conversion may be aided by dermal fibroblasts that are frequently lodged around deposits of amyloid.

摘要

对6例淀粉样变苔藓的超微结构进行了研究,特别关注表皮角质形成细胞以及张力细丝作为淀粉样原纤维前体的作用。通过凋亡过程,角质形成细胞发生变性,变成丝状细胞,然后形成丝状团块或西瓦特小体。这些小体随后通过受损的基底膜落入真皮。在乳头层真皮中,淀粉样岛与西瓦特小体紧密相连。在某些病例中,在呈涡状、紧密堆积的丝状团块内发现了向淀粉样原纤维特征性的直的无分支细丝的转变。在表皮中的角质形成细胞或西瓦特小体中未观察到向淀粉样原纤维的转变。这种最后的转变步骤可能由经常位于淀粉样沉积物周围的真皮成纤维细胞辅助完成。

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Lichen amyloidosus. Ultrastructure and pathogenesis.淀粉样变苔藓。超微结构与发病机制。
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2
Proteomic analysis shows that the main constituent of subepidermal localised cutaneous amyloidosis is not galectin-7.蛋白质组学分析表明,皮下局限性皮肤淀粉样变的主要成分不是半乳糖凝集素-7。
Amyloid. 2021 Mar;28(1):35-41. doi: 10.1080/13506129.2020.1811962. Epub 2020 Sep 1.