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脱发性毛囊炎的免疫发病机制:早期病变中的线索

Immunopathogenesis of folliculitis decalvans: clues in early lesions.

作者信息

Chiarini Caterina, Torchia Daniele, Bianchi Beatrice, Volpi Walter, Caproni Marzia, Fabbri Paolo

机构信息

Department of Dermatological Sciences, University of Florence, Florence, Italy.

出版信息

Am J Clin Pathol. 2008 Oct;130(4):526-34. doi: 10.1309/NG60Y7V0WNUFH4LA.

DOI:10.1309/NG60Y7V0WNUFH4LA
PMID:18794044
Abstract

Folliculitis decalvans (FD) is a rare variant of primary cicatricial alopecia, for which the etiopathogenesis remains unclear. Our purpose was to evaluate whether certain immunologic mechanisms might have a significant role in the pathogenesis of FD. Lesional scalp biopsy specimens from 7 patients with FD, 7 with lichen planopilaris, and 4 with alopecia areata were studied immunohistochemically by using monoclonal antibodies to CD1a, CD3, CD4, CD8, CD20, CD25, HLA-DR, interleukin (IL)-1beta, IL-4, IL-8, interferon gamma, tumor necrosis factor alpha, basic fibroblast growth factor (b-FGF), transforming growth factor (TGF)-beta, endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule. We showed that early FD lesions are characterized by an infiltration of activated T-helper cells, featuring mixed TH1/TH2 polarization. IL-8 and ICAM-1 may contribute to the infiltration of neutrophils, whereas b-FGF and TGF-beta may represent important mediators of the fibrosis that characterizes late-phase FD.

摘要

脱发性毛囊炎(FD)是原发性瘢痕性脱发的一种罕见类型,其发病机制尚不清楚。我们的目的是评估某些免疫机制是否可能在FD的发病机制中起重要作用。我们使用针对CD1a、CD3、CD4、CD8、CD20、CD25、HLA-DR、白细胞介素(IL)-1β、IL-4、IL-8、干扰素γ、肿瘤坏死因子α、碱性成纤维细胞生长因子(b-FGF)、转化生长因子(TGF)-β、内皮白细胞黏附分子1、细胞间黏附分子(ICAM)-1和血管细胞黏附分子的单克隆抗体,对7例FD患者、7例扁平苔藓样糠疹患者和4例斑秃患者的病变头皮活检标本进行了免疫组织化学研究。我们发现,早期FD病变的特征是活化的辅助性T细胞浸润,呈现TH1/TH2混合极化。IL-8和ICAM-1可能促进中性粒细胞浸润,而b-FGF和TGF-β可能是晚期FD特征性纤维化的重要介质。

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