Association of TNF-α Promoter Region (-308 G/A, rs1800629) Gene Polymorphism with Psoriasis Vulgaris in Northern Iran
Keywords:
Psoriasis vulgaris, TNF-α, rs1800629, Gene polymorphism, ARMS-PCR, Northern Iran.Abstract
Psoriasis is a chronic inflammatory skin disease with an immunogenetic background and is prevalent among various ethnic groups worldwide. The prevalence of psoriasis varies across different geographic regions and is estimated to affect approximately 2–4% of the population in Western countries. Genetic factors, including single nucleotide polymorphisms (SNPs), play important roles in the age of disease onset, clinical manifestations, disease subtype, and severity. Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine involved in systemic inflammation and is considered a key regulator of the inflammatory response. Therefore, the present study aimed to investigate the association between the TNF-α promoter region polymorphism (-308 G/A, rs1800629) and psoriasis vulgaris in populations from western Mazandaran and eastern Guilan provinces in northern Iran.
In this case–control study, whole blood samples were collected from 50 patients with psoriasis vulgaris residing in western Mazandaran and eastern Guilan, northern Iran, whose diagnosis had been confirmed by a dermatologist. Additionally, 30 whole blood samples were obtained from healthy individuals who met the inclusion criteria for the control group. Samples were collected from clinical laboratories located in the study regions. Genomic DNA was extracted from all samples, and genotyping of the TNF-α promoter region polymorphism (-308 G/A, rs1800629) was performed using the Amplification Refractory Mutation System–Polymerase Chain Reaction (ARMS-PCR) method. To validate the genotyping results and ensure the accuracy of the analysis, selected samples were further confirmed by DNA sequencing.
he results of the statistical analyses revealed that the GG genotype (homozygous dominant) was the only genotype detected in both the patient and control groups. No individuals carrying the AA (homozygous recessive) or GA (heterozygous) genotypes were identified in either group. Consequently, the frequency of the A allele was zero in the study population.
Overall, the findings demonstrated no significant difference in genotype or allele distribution between patients with psoriasis and healthy controls. Therefore, no statistically significant association was observed between the TNF-α rs1800629 polymorphism and susceptibility to psoriasis vulgaris in the studied population. Based on these results, this polymorphism cannot be considered a reliable genetic marker for the diagnosis or prediction of psoriasis in this region. Nevertheless, further studies involving larger sample sizes and broader populations are required to confirm these findings and clarify the potential role of this polymorphism in psoriasis pathogenesis.