APRIL gene polymorphism and serum sAPRIL levels in children with systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is a multi-factor autoimmune disorder with diverse clinical manifestations and unclear pathogenesis. Genetic components play important roles in the incidence and development of SLE. Among these, APRIL as a cytokine has roles in the stimulation and antibody production in B cells. APRIL was hypothesized to be associated with SLE. The aim of this study was to assess the involvement of the APRIL gene in SLE susceptibility in Iranian patients. A single-nucleotide polymorphism (SNP) for rs11552708 of APRIL gene was analyzed by real-time PCR in 60 SLE Iranian children and 64 healthy controls. DNA samples of patients and healthy controls were extracted from peripheral blood leukocytes by phenol-chloroform. Serum samples obtained from 45 children with SLE and 45 healthy controls were assayed by enzyme-linked immunosorbent assay (ELISA). The G/G genotype (odds ratio (OR) 0.67, 95% confidence interval (CI) 0.22-2.07; P = 0.68) and G allele (OR 0.81, 95% CI 0.25-2.56; P = 0.89) frequencies of polymorphism at codon 67 (67G) do not differ significantly in the SLE patients compared with those in the healthy controls. The serum APRIL levels in the SLE patients (mean ± SD = 29.27 ng/ml ± 20.77, range from 0 to 55.33 ng/ml) were significantly higher than those in the healthy controls (P = 0.02). Our results demonstrated that rs11552708 of the APRIL gene is not associated with SLE susceptibility in Iranian children. Likewise, these findings suggest that APRIL antagonist could be a potential therapeutic target to control SLE in children.

Genetic and molecular biology of systemic lupus erythematosus among Iranian patients: an overview

“…Heparin sulfate have been also reported as APRIL receptor [104][105][106]. There was significant increased serum APRIL levels in a sample of Iranian children with SLE compared with healthy cases [107]. Estrogen inhibits the apoptosis in PBMCs of SLE patients and ERα up regulation have been observed among SLE cases [108,109].…”

Single Nucleotide Polymorphism in Deoxyribonuclease I (DNase I, Q222R/rs1053874 A/G) is associated with Systemic Lupus Erythematosus (SLE)

“…Disease onset and severity are in uenced by genetic, environmental, and hormonal causes. Because of the broad variety of symptoms, SLE takes an unpredictable path (Camicia et al 2016;Namazi et al 2017). In Lupus, genomewide association studies (GWAS) have been associated with several genes linked to immune response and a consistent link to the disease (Bodan´o et al 2006).…”