Bhardwaj Supriya, Rani Seema, Srivastava Niharika, Kumar Ravinder, Parsad Davinder
Department of Dermatology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Department of Zoology, Panjab University, Chandigarh, India.
Cytokine. 2017 Mar;91:153-161. doi: 10.1016/j.cyto.2016.12.014. Epub 2017 Jan 9.
Non-segmental vitiligo (NSV) results from autoimmune destruction of melanocytes. The altered levels of various cytokines have been proposed in the pathogenesis of vitiligo. However, the exact immune mechanisms have not yet been fully elucidated.
To investigate the role of epidermal and systemic cytokines in active and stable NSV patients.
Serum levels of inflammatory cytokines were checked in 42 active and 30 stable NSV patients with 30 controls. The lesional, perilesional and normal skin sections were subjected to H&E staining. The mRNA expression of inflammatory cytokines and their respective receptors were assessed by quantitative PCR in lesional skin of both active and stable NSV skin. The MITF and IL-17A were immunolocalized in lesional, perilesional and normal skin tissue.
Significant increase in the expression of inflammatory cytokines, IL-17A, IL-1β and TGF-β was observed in active patients, whereas no change was observed in stable patients. A marked reduction in epidermal thickness was observed in lesional skin sections. Significant increase in IL-17A and significant decrease in microphthalmia associated transcription factor (MITF) expression was observed in lesional and perilesional skin sections. Moreover, qPCR analysis showed significant alterations in the mRNA levels of IL-17A, IL-1β, IFN-γ, TGF-β and their respective receptors in active and stable vitiligo patient samples.
Increased levels of IL-17A and IL-1β cytokines and decreased expression of MITF suggested a possible role of these cytokines in dysregulation of melanocytic activity in the lesional skin and hence might be responsible for the progression of active vitiligo.
非节段性白癜风(NSV)是由黑素细胞的自身免疫性破坏引起的。白癜风发病机制中各种细胞因子水平发生了改变。然而,确切的免疫机制尚未完全阐明。
研究表皮和全身细胞因子在活动期和稳定期NSV患者中的作用。
检测42例活动期和30例稳定期NSV患者以及30例对照者血清中炎症细胞因子水平。对皮损、皮损周围和正常皮肤切片进行苏木精-伊红染色。通过定量PCR评估活动期和稳定期NSV皮损皮肤中炎症细胞因子及其各自受体的mRNA表达。在皮损、皮损周围和正常皮肤组织中对小眼畸形相关转录因子(MITF)和白细胞介素-17A(IL-17A)进行免疫定位。
活动期患者炎症细胞因子IL-17A、IL-1β和转化生长因子-β(TGF-β)表达显著增加,而稳定期患者未见变化。在皮损皮肤切片中观察到表皮厚度明显降低。在皮损和皮损周围皮肤切片中观察到IL-17A显著增加,小眼畸形相关转录因子(MITF)表达显著降低。此外,定量PCR分析显示活动期和稳定期白癜风患者样本中IL-17A、IL-1β、干扰素-γ(IFN-γ)、TGF-β及其各自受体的mRNA水平有显著改变。
IL-17A和IL-1β细胞因子水平升高以及MITF表达降低表明这些细胞因子可能在皮损皮肤黑素细胞活性失调中起作用,因此可能是活动期白癜风进展的原因。