Abstract
Background: Evidence suggests that DNA damage is implicated in the development of Systemic Lupus Erythematosus (SLE). Objective: Investigate the possible association of polymorphisms in the DNA repair genes XRCC1 and XRCC3 with SLE and its clinical and laboratory features. Methods: This is a case-control study comparing the polymorphisms in the DNA repair genes XRCC1 and XRCC3 in SLE patients and control individuals. Genotyping for DNA repair genes was performed by polymerase chain reaction-restriction fragment length polymorphism in 76 patients and 82 healthy control individuals. Results: Our data indicated that the genotype frequencies in patients with the XRCC1 Arg399Gln and XRCC3 Thr241Met polymorphisms were similar to those observed in the control group (p > 0.05). However, the frequencies of the 399Gln allele (p = 0.023, OR = 0.58, 95% CI = 0.36–0.93) and 241Met allele (p = 0.0039, OR = 0.59, 95% CI = 0.36–0.98) were significantly lower in the patients than those in the control subjects. Conclusion: We demonstrated that 399Gln and 241Met alleles may play a protective role in SLE susceptibility.
Highlights
IntroductionSystemic Lupus Erythematosus (SLE) is a complex, autoimmune and chronic inflammatory disease characterized
We evaluated 76 women patients and 82 control subjects from whom we could amplify XRCC1 and XRCC3
Regarding Hardy–Weinberg equilibrium, a balance in both patients and controls was observed for both XRCC1 and XRCC3 polymorphisms
Summary
Systemic Lupus Erythematosus (SLE) is a complex, autoimmune and chronic inflammatory disease characterized. 16 The Open Rheumatology Journal, 2019, Volume 13 factors and genetic susceptibility [6, 7]. SLE can be considered a multifactorial disease since genetic susceptibility, hormonal and environmental factors can influence the immunological abnormalities observed in these patients [4]. Exogenous hormone use is associated with a high risk of SLE. Exposure to respirable silica dust and smoking have been defined as risk factors for SLE. Defective immune regulatory mechanisms caused by genetic mutations or single nucleotide polymorphisms can dysregulate inflammatory cytokine production and the clearance of apoptotic cells or immune complexes [1, 4, 5, 8 - 10]. Evidence suggests that DNA damage is implicated in the development of Systemic Lupus Erythematosus (SLE)
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