Farrell A M, Dean D, Millard P R, Charnock F M, Wojnarowska F
Department of Dermatology, Oxford Radcliffe Hospitals, Oxford, UK.
Br J Dermatol. 2006 Nov;155(5):931-40. doi: 10.1111/j.1365-2133.2006.07414.x.
Although the histology of lichen sclerosus is characteristic, the precise nature of the inflammatory changes and the signals provoking them is uncertain.
To delineate the inflammatory changes in lichen sclerosus more accurately by studying cytokine changes.
An immunohistochemical study of 12 specimens of genital lichen sclerosus and one specimen of extragenital lichen sclerosus was undertaken using monoclonal antibodies to interferon (IFN)-gamma, IFN-gamma receptor, tumour necrosis factor (TNF)-alpha, interleukin (IL)-1alpha, IL-2 receptor (CD25), intercellular adhesion molecule-1 (ICAM-1) and its ligand CD11a. Control specimens were seven specimens of normal vulva obtained during gynaecological procedures, three specimens of normal skin, adjacent uninvolved thigh from three of the patients with lichen sclerosus, five specimens of nonvulval psoriasis, four specimens of nonvulval lichen planus and two specimens from chronic wounds.
The lichen sclerosus specimens demonstrated slightly increased staining for IFN-gamma within the epidermis compared with the normal vulva and nonvulval skin. There was increased dermal staining for IFN-gamma both within the pale zone of the upper dermis and within the inflammatory zone below this. We confirmed our previous demonstration that in lichen sclerosus HLA-DR immunostaining is increased in association with vascular endothelium, the inflammatory cell infiltrate and around the keratinocytes. The areas of the epidermis with the strongest immunostaining for HLA-DR generally also had the strongest staining for IFN-gamma. In the lichen sclerosus specimens the zone of inflammation also demonstrated increased immunostaining for TNF-alpha, IL-1alpha, IFN-gamma receptor, CD25, CD11a and ICAM-1 while the zone of sclerosus demonstrated a smaller increase in immunostaining for IFN-gamma receptor, TNF-alpha, CD11a and ICAM-1, and the epidermis demonstrated increased staining for ICAM-1.
The increased staining for IFN-gamma, TNF-alpha, IL-1alpha, IFN-gamma receptor, CD25, CD11a and ICAM-1 suggest that the cytokine response in lichen sclerosus shares characteristics of the cytokine response in lichen planus and chronic wounds.
尽管硬化性苔藓的组织学表现具有特征性，但炎症变化的确切性质以及引发这些变化的信号尚不确定。
通过研究细胞因子变化更准确地描绘硬化性苔藓的炎症变化。
使用针对干扰素（IFN）-γ、IFN-γ受体、肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1α、IL-2受体（CD25）、细胞间黏附分子-1（ICAM-1）及其配体CD11a的单克隆抗体，对12例生殖器硬化性苔藓标本和1例生殖器外硬化性苔藓标本进行免疫组织化学研究。对照标本包括7例妇科手术中获取的正常外阴标本、3例正常皮肤标本、3例硬化性苔藓患者相邻未受累大腿的皮肤标本、5例非外阴部银屑病标本、4例非外阴部扁平苔藓标本以及2例慢性伤口标本。
与正常外阴和非外阴部皮肤相比，硬化性苔藓标本的表皮内IFN-γ染色略有增加。在上层真皮的浅色区域以及其下方的炎症区域内，真皮内IFN-γ染色均增加。我们证实了之前的研究结果，即在硬化性苔藓中，HLA-DR免疫染色在血管内皮、炎症细胞浸润以及角质形成细胞周围增加。HLA-DR免疫染色最强的表皮区域通常IFN-γ染色也最强。在硬化性苔藓标本中，炎症区域对TNF-α、IL-1α、IFN-γ受体、CD25、CD11a和ICAM-1的免疫染色也增加，而硬化区域对IFN-γ受体、TNF-α、CD11a和ICAM-1的免疫染色增加较少，表皮对ICAM-1的染色增加。
IFN-γ、TNF-α、IL-1α、IFN-γ受体、CD25、CD11a和ICAM-1染色增加表明，硬化性苔藓中的细胞因子反应具有扁平苔藓和慢性伤口中细胞因子反应的特征。
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