Abstract
BackgroundIt has been confirmed that tumor necrosis factor-alpha (TNFα), a macrophage-derived pro-inflammatory cytokine, plays an important role in the pathogenesis of psoriasis vulgaris and psoriatic arthritis (PsV&PsA). In contrast, the reported association of TNFα gene promoter region single nucleotide polymorphisms (SNPs) and PsV&PsA has remained controversial. Accordingly, we performed a meta-analysis to provide new evidence that SNPs in the TNFα gene promoter region alter not only the risk of psoriasis vulgaris (PsV) or psoriatic arthritis (PsA) but also of PsV&PsA.MethodsInterrelated literature dated to October 2012 was acquired from the PubMed, ScienceDirect, and SpringerLink databases. The number of the genotypes and/or alleles for the TNFα promoter in the PsV and PsA and control subjects was obtained. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to calculate the risk of PsV and/or PsA with TNFα promoter SNPs.ResultsA total of 26 papers of 2159 for PsV (2129 normal controls) and 2360 for PsA (2997 normal controls) were included in our meta-analysis. The results showed that the variant genotype and allele of TNFα -308A/G was protective in pooled groups of patients with PsV&PsA (OR = 0.682, 0.750; 95% CI, 0.596-0.779, 0.653-0.861). However, the variant genotypes and alleles of TNFα -238A/G and -857T/C had an increased risk of PsV&PsA (OR = 2.493, 2.228, 1.536, 1.486, 95% CI, 1.777-3.498, 1.628-3.049, 1.336-1.767, 1.309-1.685). Moreover, the meta-analysis revealed a significant association between TNFα -238A/G and -857T/C polymorphism and PsA susceptibility (OR = 2.242, 2.052, 1.419, 1.465; 95% CI, 1.710-2.941, 1.614-2.610, 1.214-1.658, 1.277-1.681). In contrast, the variant genotypes and alleles of TNFα -308A/G proved to be protective against PsV (OR = 0.574, 0.650, 95% CI, 0.478-0.690, 0.556-0.759), whereas TNFα -238A/G was found to have a risk association (OR = 2.636, 2.223, 95% CI, 1.523-4.561, 1.317-3.751).ConclusionsSNPs in the TNFα gene promoter region alter the risk of PsV and/or PsA.
Highlights
Psoriasis is a common autoimmune disorder that primarily involves the skin
Caution should be exercised when interpreting the results of this meta-analysis. This meta-analysis confirms the previous results that tumor necrosis factor-alpha (TNFa) 238A/G and TNFa -308A/G polymorphisms are associated with psoriasis vulgaris (PsV) or psoriatic arthritis (PsA) susceptibility
This meta-analysis shows that the TNFa -857T/C variant increases the risk of PsA significantly, whereas TNFa -857T/C and TNFa -238A/G polymorphisms are risk effects in the pooled analysis of PsV & PsA
Summary
Psoriasis is a common autoimmune disorder that primarily involves the skin (psoriasis vulgaris, PsV). Under the category of genetic and environmental effects, cytokines, chemokines, adhesion molecules, and growth factors combined with T cells and dendritic cells act in an integrated manner to evolve into unique inflammatory and proliferative processes in psoriasis vulgaris and psoriatic arthritis (PsV & PsA) [1]. It has been confirmed that tumor necrosis factor-alpha (TNFa), a macrophage-derived pro-inflammatory cytokine, plays an important role in the pathogenesis of psoriasis vulgaris and psoriatic arthritis (PsV&PsA). The reported association of TNFa gene promoter region single nucleotide polymorphisms (SNPs) and PsV&PsA has remained controversial. We performed a meta-analysis to provide new evidence that SNPs in the TNFa gene promoter region alter the risk of psoriasis vulgaris (PsV) or psoriatic arthritis (PsA) and of PsV&PsA
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.