血清 IFN-γ 和 IL-10 作为白癜风疾病活动性预测生物标志物的作用:病例对照研究

Karishma Desai, H. Yadalla
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引用次数: 0

摘要

IFNγ是一种多效细胞因子,通过调控免疫相关基因,它们能协调多种细胞程序[1]。作为一种强效促炎细胞因子,IFNγ在诱导白癜风患者色素脱失方面发挥着关键作用。在本研究中,我们旨在评估 IFNγ 在疾病的活动、持续时间和程度中的作用,同时评估 IL-10 在白癜风中的拮抗作用。 这项病例对照研究有 100 名参与者参加,其中 50 例经临床诊断为白癜风,50 例为对照组。所有患者都接受了全面的评估,包括详细的人口统计学参数、病史和体格检查。临床上通过白癜风面积评分指数(VASI)和白癜风疾病活动度评分(VIDA)来评估疾病的严重程度。血液检查包括 IFN-γ 和 IL-10。 我们观察到,与正常对照组相比,患者组的血清 IFNγ 水平明显较高(p=0.002),并且与疾病的活动性和严重程度呈正相关,VASI(p=0.05)和 VIDA 评分(p=<0.001)显著。白癜风患者的平均血清IL-10(p<0.001)明显低于对照组。 这项研究显示,IFN-γ 的血清水平明显较高,而 IL-10 的水平则相应较低。IFN-γ阻断与其他信号通路抑制相结合等新策略可能会进一步改善该疾病的IFN-γ靶向免疫疗法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of Serum IFN-γ and IL-10 as Predictive Biomarkers of Vitiligo Disease Activity: A Case-Control Study
IFNγ is a pleiotropic cytokine and through the regulation of immunologically relevant genes, they coordinate a wide range of cellular programs.[1] As a potent pro-inflammatory cytokine, it plays a pivotal role to induce depigmentation in vitiligo. In this study, we aim to assess the role of IFNγ in the activity, duration and extent of the disease and the antagonistic action of IL-10 is also assessed in vitiligo. A case-control study was conducted with 100 study participants with 50 cases clinically diagnosed as Vitiligo and 50 controls. All patients underwent complete evaluation with detailed demographic parameters, history and physical examination. The severity of the disease was assessed clinically by Vitiligo Area Scoring Index (VASI) and Vitiligo Disease Activity Score (VIDA). And blood investigations done were IFN-γ and IL-10. We observed significantly higher levels of serum IFNγ levels in the patient group when compared with those of the normal controls (p=0.002) and showed a positive correlation with the activity and severity of the disease with a significant VASI (p=0.05) and VIDA score (p=<0.001). The mean serum IL-10 (p<0.001) in patients with vitiligo was significantly lower than that in the control group. This study showed significantly high serum levels of IFN-γ and correspondingly low levels of IL-10. New strategies, such as the combination of IFNγ blockade with inhibition of other signalling pathways, may further improve IFNγ targeted immunotherapy of the disease.
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