外阴硬化及萎缩性地衣皮肤免疫系统受累的免疫组化证据。

Dermatologica Pub Date : 1991-01-01 DOI:10.1159/000247730
P Carli, A Cattaneo, N Pimpinelli, A Cozza, G Bracco, B Giannotti
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引用次数: 46

摘要

对12例患有外阴硬化性地衣萎缩(LSA)的女性外阴病变进行了活检,并进行了免疫组织学研究。所有病例的真皮中均发现活化的(HLA-Dr+) T细胞与CD1a+辅助细胞相关,其结构模式随病变的组织学阶段(早期、发育良好、老)而变化。有趣的是,在所有病例中,表皮CD1a+朗格汉斯细胞(LCs)的数量都增加了,与真皮浸润的数量和病变的组织学阶段没有任何关系。事实上,同样在老年病变中,表皮CD1a+ lccs的数量增加,稀疏的真皮淋巴样细胞持续表达HLA-Dr抗原。这些数据表明,在外阴LSA的所有进化阶段,表皮抗原呈递细胞和淋巴样细胞持续激活,提示皮肤免疫系统可能参与了LSA的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immunohistochemical evidence of skin immune system involvement in vulvar lichen sclerosus et atrophicus.

Biopsies taken from vulvar lesions in 12 women affected by vulvar lichen sclerosus et atrophicus (LSA) have been processed for immunohistological study. Activated (HLA-Dr+) T cells, associated with CD1a+ accessory cells, were found in the dermis in all cases, with architectural patterns varying in relation to the histological phase (early, well developed, old) of the lesion. Interestingly, the number of epidermal CD1a+ Langerhans cells (LCs) was increased in all cases, without any correlation with the amount of the dermal infiltrate and with the histological phase of the lesions. In fact, also in old lesions the number of epidermal CD1a+ LCs was increased, and the sparse dermal lymphoid cells showed a persistent HLA-Dr antigen expression. These data, indicating the persistent activation of epidermal antigen-presenting cells and lymphoid cells in all the evolutive phases of vulvar LSA, suggest a possible involvement of the skin immune system in the pathogenesis of LSA.

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