Melatonin Receptor 1β Gene Polymorphism rs10830963, Serum Melatonin, TNF-α, IL-6, IL-1β, in Egyptian Patients with Systemic Lupus Erythematosus.

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.