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晕痣炎症细胞浸润中CD69的表达及肿瘤坏死因子-α免疫反应性

CD69 expression and tumour necrosis factor-alpha immunoreactivity in the inflammatory cell infiltrate of halo naevi.

作者信息

Fernández-Herrera J, Fernández-Ruiz E, López-Cabrera M, García-Díez A, Sánchez-Madrid F, González-Amaro R

机构信息

Servicios de Dermatología, Universidad Autónoma de Madrid, Spain.

出版信息

Br J Dermatol. 1996 Mar;134(3):388-93.

PMID:8731658
Abstract

It has been suggested that the involution of the pigmented lesions of halo naevus (HN) is mediated by an immune response, with the involvement of specific cytotoxic T lymphocytes. To explore further the pathogenesis of HN, skin biopsies from six patients with this condition were obtained and the characteristics of the infiltrating inflammatory cells were studied by immunostaining techniques. We found that the cell infiltrate of HN is mainly composed by CD8+ T lymphocytes that express the activation molecule CD69. Tumour necrosis factor-alpha (TNF-alpha) immunoreactivity was detected on the inflammatory cells, a finding that suggests that the infiltrating T cells of HN are actively synthesizing this cytokine. Our results indicate that the infiltrating cells of HN predominantly have an activated cytotoxic phenotype, and suggest that these cells are indeed involved in the regression of the naevomelanocytic naevus of HN.

摘要

有人提出晕痣(HN)色素沉着病变的消退是由免疫反应介导的,涉及特定的细胞毒性T淋巴细胞。为了进一步探讨HN的发病机制,获取了6例患有此病患者的皮肤活检样本,并通过免疫染色技术研究了浸润性炎症细胞的特征。我们发现,HN的细胞浸润主要由表达激活分子CD69的CD8 + T淋巴细胞组成。在炎症细胞上检测到肿瘤坏死因子-α(TNF-α)免疫反应性,这一发现表明HN浸润性T细胞正在积极合成这种细胞因子。我们的结果表明,HN的浸润细胞主要具有活化的细胞毒性表型,并表明这些细胞确实参与了HN痣细胞痣的消退。

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