ABSTRACT
Background and Aim: Systemic lupus erythematosus [SLE] is an autoimmune disease that is characterized by the presence of autoantibodies against nuclear antigens. The exact cause of SLE is unknown, but some of these genes are active in the key pathways, including immune complexes, host immune signal transduction, and interferon pathways which have significant roles in the pathogenesis of SLE. Since the classical HLA class I and II molecules are highly involved in the peptide presentation to the components of immune system, the genes that encode these molecules can be primary candidates associated with susceptibility to autoimmune disorders. HLA-G belongs to the family of non-classical HLA class I antigens. The purpose of this study was to evaluate the association of INDEL polymorphism of the 3'UTR region of HLA-G gene with SLE
Material and Methods: In this study, 80 patients with SLE, and 102 healthy individuals were examined. Genomic DNA was extracted from peripheral blood. The genotypes were determined using ARMS-PCR. Data analysis was performed using MedCalc version 12.1
Results: The frequencies of homozygot genotypes for the presence of [+14bp/+14bp]14bp, hetrozygot genotypes for [-14bp/+14bp], and homozygot genotypes with deletion of [-14bp/-14bp]14bp segments in the healthy individuals were 21.57%, 41.18% and 37.25%, and in the patients were 17.5%, 42.5% and 40% respectively. The most frequent genotype in the healthy individuals and hetrozygot patients was [-14bp/+14bp]. We found no statistically significant differences in the genotype distributions between the cases and controls [and Rho;>0.05]
Conclusion: In this study INDEL polymorphism of the 3UTR region of HLA-G gene showed no association with systemic lupus erythematosus. However, further studies are required to confirm the validity of these results