Genetic association between TNF-α −857 C/T polymorphism and ankylosing spondylitis susceptibility: evidence from a meta-analysis

Abstract

Certain studies have suggested that the tumor necrosis factor-α (TNF-α) −857 C/T polymorphism is associated with risk of ankylosing spondylitis. However, the conclusions remain controversial. Therefore, we performed a meta-analysis to provide a more precise conclusion. Such databases as PubMed, Embase, CBM, CNKI, and Wanfang Data were searched to identify relevant studies up to August 26, 2015. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the association between TNF-α −857 C/T polymorphism and ankylosing spondylitis susceptibility. A total of 10 studies were included in the meta-analysis. Overall, an elevated risk between TNF-α −857 C/T polymorphism and ankylosing spondylitis was observed in three genetic model (T vs. C: OR 1.86, 95% CI 1.19–2.92; CT vs. CC: OR 2.51, 95% CI 1.49–4.23; TT + CT vs. CC: OR 2.46, 95% CI 1.40–4.30), except in homozygote model (TT vs. CC: OR 2.41, 95% CI 0.96–6.06) and recessive model (TT vs. CT + CC: OR 1.54, 95% CI 0.71–3.35). Sensitivity analysis showed the overall results were robust. Subgroup analyses according to Hardy–Weinberg equilibrium and ethnicity showed that the increased risk of ankylosing spondylitis were predominant in Asian population. This meta-analysis indicated that TNF-α −857 C/T polymorphism might increase the susceptibility of ankylosing spondylitis, especially in Asians. Further studies were needed to verify the conclusion.

Association of CARD10 rs6000782 and TNF rs1799724 variants with paediatric-onset autoimmune hepatitis

“…The present study reveals that compared with the CC genotype, the rs1799724 CT genotype is a risk factor for pAIH. Despite conflicting data regarding rs17999724 and autoimmune diseases, the findings agree with meta-analyses of diseases such as ankylosing spondylitis [20], Crohn’s disease [21] and vitiligo [18] using additive, dominant, and allele models. In contrast, a lack of this association was documented for idiopathic nephrotic syndrome [30] and rheumatoid arthritis [31].…”

“…Overexpression of TNF-α in AIH patients’ sera has been reported, with the level directly correlating with prognosis [19]. In addition, the TNF promoter polymorphism rs1799724 (c.-1037C > T) has been associated with autoimmune diseases, such as ankylosing spondylitis and Crohn’s disease [20], [21] and with susceptibility to hepatitis B virus infection in some populations [22].…”

Genetics and Extracellular Vesicles of Pediatrics Sleep Disordered Breathing and Epilepsy

“…Several studies have reported the potential of miRNAs as biomarkers for different aspects of the epileptogenic process [141,142]. Recent studies have reported that the associations of miRNAs and SNPs, one of which in childhood of epilepsy [143], and the relation to drug-resistance [144]. Here, we show for the first time the number of miRNAs that targeting the CYP2C19 gene, which includes the following: hsa-miR-1270, hsa-miR-455-3p, hsa-miR-4325, hsa-miR-7703, hsa-miR-6880-5p, hsa-miR-6851-5p, hsa-miR-3689d, hsa-miR-4683, hsa-miR-6499-3p, hsa-miR-767-5p, hsa-miR-6134, hsa-miR-4537, hsa-miR-5186, hsa-miR-665, hsa-miR-4459, hsa-miR-92b-3p, hsa-miR-92a-3p, hsa-miR-367-3p, hsa-miR-363-3p, hsa-miR-32-5p, hsa-miR-25-3p, hsa-miR-3180-5p, hsa-miR-3912-5p, hsa-miR-874-3p, hsa-miR-3157-3p, hsa-miR-5195-3p, hsa-miR-145-5p, and hsa-miR-6886-3p.…”

Comparison of Incidence or Recurrence of Anterior Uveitis in Patients with Ankylosing Spondylitis Treated with Tumor Necrosis Factor Inhibitors

“…TNFi block the activity of TNFα, a key inflammatory mediator as a pro-inflammatory cytokine. Several studies have established a significant relationship between TNFα and AS [4][5][6][7][8]. TNFα is known to play a crucial role in the pathogenesis of AS, as it is overproduced in AS predominantly by active macrophages and T-lymphocytes, playing key roles in the inflammation of spine and sacroiliac joints and extra-articular manifestations including uveitis [4,5].…”

“…TNFα is known to play a crucial role in the pathogenesis of AS, as it is overproduced in AS predominantly by active macrophages and T-lymphocytes, playing key roles in the inflammation of spine and sacroiliac joints and extra-articular manifestations including uveitis [4,5]. Genetic association studies have evaluated the link between TNFα polymorphisms and susceptibility to AS, indicating a potential genetic influence on the development of the disease [6]. Furthermore, the efficacy of TNFα inhibitors for the treatment of AS has been demonstrated, highlighting the therapeutic relevance of targeting TNFα in managing AS [7,8].…”