PDF(Pubmed)
Abstract：
UNASSIGNED: Vulvar lichen sclerosus (VLS) is a chronic progressive, lymphocyte-mediated inflammatory disease whose pathogenesis is complex and not fully elucidated.
UNASSIGNED: In the current study we have investigated for the first time the expression of interleukin-17 (IL-17) and S100A7 in lesional skin obtained from female individuals with histologically confirmed VLS.
UNASSIGNED: In our study we used skin biopsies obtained from female patients with histologically confirmed VLS (n = 20) and skin samples from healthy age- and gender-matched individuals (plastic surgery procedures) (n = 10) serving as controls. The tissue expressions of IL-17 and S100A7 were assessed with an immunohistochemical method.
UNASSIGNED: The number of cells showing IL-17 expression was significantly higher in VLS lesional skin as compared to normal skin of healthy controls (p < 0.0001). In VLS lesional skin, IL-17 was expressed in the epidermis and by cells within the inflammatory infiltrate in the upper dermis. The number of cells showing S100A7 expression was significantly higher in VLS lesional skin as compared to normal skin of healthy controls (p < 0.0001). In VLS lesional skin, S100A7 was expressed by suprabasal keratinocytes in epidermis. S100A7 was also expressed by cells within the inflammatory infiltrate in the dermis.
UNASSIGNED: The results of our study may suggest the involvement of IL-17 and S100A7 in the pathogenesis of VLS. The better understanding of this disease may lead to the development of novel, effective therapeutic strategies e.g. using well-known biologics IL-17 inhibitors class.
UNASSIGNED: In the current study we have investigated for the first time the expression of interleukin-17 (IL-17) and S100A7 in lesional skin obtained from female individuals with histologically confirmed VLS.
UNASSIGNED: In our study we used skin biopsies obtained from female patients with histologically confirmed VLS (n = 20) and skin samples from healthy age- and gender-matched individuals (plastic surgery procedures) (n = 10) serving as controls. The tissue expressions of IL-17 and S100A7 were assessed with an immunohistochemical method.
UNASSIGNED: The number of cells showing IL-17 expression was significantly higher in VLS lesional skin as compared to normal skin of healthy controls (p < 0.0001). In VLS lesional skin, IL-17 was expressed in the epidermis and by cells within the inflammatory infiltrate in the upper dermis. The number of cells showing S100A7 expression was significantly higher in VLS lesional skin as compared to normal skin of healthy controls (p < 0.0001). In VLS lesional skin, S100A7 was expressed by suprabasal keratinocytes in epidermis. S100A7 was also expressed by cells within the inflammatory infiltrate in the dermis.
UNASSIGNED: The results of our study may suggest the involvement of IL-17 and S100A7 in the pathogenesis of VLS. The better understanding of this disease may lead to the development of novel, effective therapeutic strategies e.g. using well-known biologics IL-17 inhibitors class.
摘要：
■硬化外阴苔藓（VLS）是一种慢性进行性，淋巴细胞介导的炎症性疾病，其发病机制复杂且尚未完全阐明。
■在当前的研究中，我们首次研究了从组织学证实的VLS的女性个体获得的病灶皮肤中白介素17（IL-17）和S100A7的表达。
在我们的研究中,我们使用从具有组织学证实的VLS的女性患者获得的皮肤活检(n=20)和来自健康的年龄和性别匹配的个体(整形外科程序)的皮肤样本(n=10)作为对照。用免疫组织化学方法评估IL-17和S100A7的组织表达。
与健康对照的正常皮肤相比,在VLS病变皮肤中显示IL-17表达的细胞数量显著更高(p<0.0001)。在VLS病变皮肤中，IL-17在表皮中和上真皮中的炎性浸润物内的细胞中表达。与健康对照的正常皮肤相比,VLS病变皮肤中显示S100A7表达的细胞数量显著更高(p<0.0001)。在VLS病变皮肤中，S100A7由表皮中的基底上角质形成细胞表达。S100A7也由真皮中的炎性浸润物内的细胞表达。
■我们的研究结果可能提示IL-17和S100A7参与了VLS的发病机制。更好地了解这种疾病可能会导致新的发展，有效的治疗策略,例如使用熟知的生物制剂IL-17抑制剂类。
■在当前的研究中，我们首次研究了从组织学证实的VLS的女性个体获得的病灶皮肤中白介素17（IL-17）和S100A7的表达。
在我们的研究中,我们使用从具有组织学证实的VLS的女性患者获得的皮肤活检(n=20)和来自健康的年龄和性别匹配的个体(整形外科程序)的皮肤样本(n=10)作为对照。用免疫组织化学方法评估IL-17和S100A7的组织表达。
与健康对照的正常皮肤相比,在VLS病变皮肤中显示IL-17表达的细胞数量显著更高(p<0.0001)。在VLS病变皮肤中，IL-17在表皮中和上真皮中的炎性浸润物内的细胞中表达。与健康对照的正常皮肤相比,VLS病变皮肤中显示S100A7表达的细胞数量显著更高(p<0.0001)。在VLS病变皮肤中，S100A7由表皮中的基底上角质形成细胞表达。S100A7也由真皮中的炎性浸润物内的细胞表达。
■我们的研究结果可能提示IL-17和S100A7参与了VLS的发病机制。更好地了解这种疾病可能会导致新的发展，有效的治疗策略,例如使用熟知的生物制剂IL-17抑制剂类。
