Fayad Amira, Hassan Eman, Salem Tarek
Department of Clinical & Chemical Pathology, Faculty of Medicine, Alexandria University, Alexandria, Egypt.
Department of Internal Medicine, Faculty of Medicine, Alexandria University, Alexandria, Egypt.
Egypt J Immunol. 2019 Jan;26(1):101-112.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease affecting all organ systems due to alterations of both innate and adaptive immune systems. Given the importance of several factors that may be incriminated in deregulation of immune system in SLE, we aimed to study MTNR1β gene polymorphisms rs10830963 C/G, serum levels of melatonin and pro-inflammatory cytokines; TNF-α, IL-6, and IL-1β in SLE patients and the correlation of these parameters to SLE disease activity and damage index at time of study. Subjects were subdivided into 2 groups: group I: 40 SLE patients attending Alexandria main university hospital and outpatient clinic, and group II: 40 control cases of apparently healthy individuals matched for age and sex. For all cases, MTNR1β gene polymorphism rs10830963 was analyzed by quantitative RT-PCR, serum levels of melatonin, TNF-α, IL-6 and IL-1β were detected by ELISA. Activity index (SLEDAI) and damage index (SLEDDI) were assessed in SLE patients. MTNR1β gene polymorphism rs10830963 genotype in SLE patients showed that 50% had GG, 35% CG and 15% CC. The control group had significantly lower ratios, 5% had GG, 15% CG and 80% CC (P < 0.001). Serum melatonin level was decreased in SLE patients (P < 0.001). Serum levels of TNF-α, IL-6, and IL-1β were increased in SLE patients compared to controls (P < 0.001, P < 0.001, P < 0.001 respectively). There was no correlation between serum melatonin level, TNF-α, IL-6, and IL-1β with SLEDAI or SLEDDI. In conclusion, MTNR1β gene polymorphism rs10830963 G allele may contribute in SLE pathogenesis. Inflammatory cytokines; TNF-α, IL-6, IL-1β may have role in SLE disease manifestations. Targeting immunoregulators as melatonin and proinflammatory cytokines in SLE treatment strategy can be a promising way to SLE cure.
系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，由于先天性和适应性免疫系统的改变，会影响所有器官系统。鉴于可能与SLE免疫系统失调有关的几个因素的重要性，我们旨在研究MTNR1β基因多态性rs10830963 C/G、褪黑素血清水平和促炎细胞因子；SLE患者体内的TNF-α、IL-6和IL-1β，以及这些参数与研究时SLE疾病活动和损伤指数的相关性。受试者分为两组：第一组：40名在亚历山大主大学医院和门诊就诊的SLE患者，第二组：40名年龄和性别相匹配的明显健康个体作为对照病例。对于所有病例，通过定量RT-PCR分析MTNR1β基因多态性rs10830963，通过ELISA检测褪黑素、TNF-α、IL-6和IL-1β的血清水平。对SLE患者评估活动指数（SLEDAI）和损伤指数（SLEDDI）。SLE患者的MTNR1β基因多态性rs10830963基因型显示，50%为GG，35%为CG，15%为CC。对照组的比例显著较低，5%为GG，15%为CG，80%为CC（P < 0.001）。SLE患者的血清褪黑素水平降低（P < 0.001）。与对照组相比，SLE患者的TNF-α、IL-6和IL-1β血清水平升高（分别为P < 0.001、P < 0.001、P < 0.001）。血清褪黑素水平、TNF-α、IL-6和IL-1β与SLEDAI或SLEDDI之间无相关性。总之，MTNR1β基因多态性rs10830963 G等位基因可能在SLE发病机制中起作用。炎性细胞因子；TNF-α、IL-6、IL-1β可能在SLE疾病表现中起作用。在SLE治疗策略中，将褪黑素和促炎细胞因子等免疫调节因子作为靶点可能是治愈SLE的一种有前景的方法。
