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口腔扁平苔藓:黏膜病变的免疫组织学

Oral lichen planus: immunohistology of mucosal lesions.

作者信息

Villarroel Dorrego Mariana, Correnti María, Delgado Rafael, Tapia Felix J

机构信息

Instituto de Investigaciones Odontológicas Raúl Vincentelli, Universidad Central de Venezuela, Caracas, Venezuela.

出版信息

J Oral Pathol Med. 2002 Aug;31(7):410-4. doi: 10.1034/j.1600-0714.2002.00097.x.

Abstract

BACKGROUND

Current evidence suggests that immunological mechanisms are involved in oral lichen planus (OLP) pathogenesis. The events implicate activated epithelia that comprise antigen-presenting Langerhans cells, immunocompetent keratinocytes and subepithelial inflammatory infiltrate. Also, the presence of a high density of leucocyte cells may occur for the expression of a variety of adhesion molecules. The aim of this study was to analyse the immunoexpression of some adhesion molecules as well as lymphocytic markers in order to determine the disease pathogenesis in a Venezuelan population.

METHODS

The 18 OLP and 10 normal oral mucosa biopsies were immunostained for CD4, CD8, CD1a, LFA-1, VCAM-1 and ICAM-1.

RESULTS

The results showed an increased number of CD4+, CD8+, CD1a+ cells in OLP. Serial sections showed CD4+ and CD8+ cells also expressed LFA-1. The expression of ICAM-1 and VCAM-1 were significantly higher in OLP.

CONCLUSIONS

The immunological reaction begins with Langerhans cells activation, which presents an antigen to CD4+ lymphocytes. Those cells through ICAM-1 and LFA-1 promote epithelial destruction. Afterwards, cytokine production, ICAM-1 and VCAM-1 expression can activate CD8+ lymphocytes leading to the chronic form of the disease.

摘要

背景

目前的证据表明免疫机制参与口腔扁平苔藓(OLP)的发病过程。这些事件涉及活化的上皮细胞,包括抗原呈递的朗格汉斯细胞、具有免疫活性的角质形成细胞和上皮下炎性浸润。此外,高密度白细胞的存在可能与多种黏附分子的表达有关。本研究的目的是分析一些黏附分子以及淋巴细胞标志物的免疫表达情况,以确定委内瑞拉人群中该疾病的发病机制。

方法

对18例OLP活检组织和10例正常口腔黏膜活检组织进行CD4、CD8、CD1a、淋巴细胞功能相关抗原-1(LFA-1)、血管细胞黏附分子-1(VCAM-1)和细胞间黏附分子-1(ICAM-1)免疫染色。

结果

结果显示OLP中CD4⁺、CD8⁺、CD1a⁺细胞数量增加。连续切片显示CD4⁺和CD8⁺细胞也表达LFA-1。OLP中ICAM-1和VCAM-1的表达显著更高。

结论

免疫反应始于朗格汉斯细胞的活化,其将抗原呈递给CD4⁺淋巴细胞。这些细胞通过ICAM-1和LFA-1促进上皮破坏。随后,细胞因子的产生、ICAM-1和VCAM-1的表达可激活CD8⁺淋巴细胞,导致疾病的慢性形式。

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