In autoimmune dermatitis patients, a macrophage migration inhibitory factor (MIF) is widely used to determine the severity of the diseases with other clinical parameters. Moreover, in vitiligo, MIF has shown significant positive correlation with the VASI (Vitiligo Area Scoring Index) score of both generalized and localized vitiligo patients. MIF function as pro-inflammatory cytokine and inhibited random migration of macrophages from inflammation loci. Hence, activated macrophage infiltrates promote the diseases pathogenesis. Till date, macrophages and involvement of their secreted MIF in disease severity of vitiligo patients remains undetermined. The frequency of both M1 and M2 macrophages was evaluated in active GV patients (n = 20) using flow cytometry in blood and in tissues by confocal microscopy (n = 10). Relative m-RNA expression and cytokine profiling of pro and anti-inflammatory mediators were estimated in PBMCs and in serum of patients. Lastly, concentration of nitric oxide and phagocytic activity from macrophages of active patients were calculated to understand the diseases pathology in detail. Both in circulation as well as in tissues, the infiltration of M1 macrophages was increased in active GV patients, while the percentage of M2 macrophages was comparable to healthy tissues. Aberrant expression of pro and anti-inflammatory molecules including IL-1β, IL-6, TNF-α, IL-12 and MIF impair the cellular hemostasis and induce systematic inflammation. Elevated nitric oxide and higher phagocytic activity of macrophages enhanced the destruction and/or depigmentation of melanocytes causing vitiligo. Elevated macrophages in both tissue and blood enhanced the secretion of MIF and other inflammatory mediators that further enforce the production of nitric oxide, activation and phagocytic activity of macrophages against melanocytes and melanocytes antigens. As a result, destruction of melanocytes and melanin production occurred and caused the depigmentation and/or white macules on the skin.

中文翻译：

---

巨噬细胞抑制因子改变巨噬细胞的功能及其参与活动性全身性白癜风患者的疾病发病机制

在自身免疫性皮炎患者中，巨噬细胞迁移抑制因子（MIF）被广泛用于结合其他临床参数来确定疾病的严重程度。此外，在白癜风中，MIF与全身性和局限性白癜风患者的VASI（白癜风面积评分指数）评分均显示出显着的正相关性。MIF 作为促炎细胞因子发挥作用，并抑制巨噬细胞从炎症位点的随机迁移。因此，活化的巨噬细胞浸润促进了疾病的发病机制。迄今为止，巨噬细胞及其分泌的 MIF 与白癜风患者疾病严重程度的关系仍不清楚。使用流式细胞术评估活动性 GV 患者 (n = 20) 血液中的 M1 和 M2 巨噬细胞频率，并通过共聚焦显微镜 (n = 10) 评估组织中 M1 和 M2 巨噬细胞的频率。评估了 PBMC 和患者血清中促炎介质和抗炎介质的相对 mRNA 表达和细胞因子谱。最后，计算活跃患者的一氧化氮浓度和巨噬细胞的吞噬活性，以详细了解疾病的病理学。在循环和组织中，活动性 GV 患者中 M1 巨噬细胞的浸润增加，而 M2 巨噬细胞的百分比与健康组织相当。促炎和抗炎分子（包括 IL-1β、IL-6、TNF-α、IL-12 和 MIF）的异常表达会损害细胞止血并诱导系统性炎症。一氧化氮升高和巨噬细胞吞噬活性升高，增强了黑素细胞的破坏和/或脱色，导致白癜风。组织和血液中巨噬细胞的升高增强了 MIF 和其他炎症介质的分泌，进一步增强了一氧化氮的产生、巨噬细胞对黑素细胞和黑素细胞抗原的激活和吞噬活性。结果，黑素细胞和黑色素产生遭到破坏，并导致皮肤上色素脱失和/或出现白斑。