Association Between TNF‐α Promoter −308 A/G Polymorphism and Systemic Lupus Erythematosus Susceptibility: A Case–Control Study and Meta‐Analysis

Abstract

The tumour necrosis factor-α (TNF-α) promoter -308 A/G polymorphism plays an important role in the aetiology of systemic lupus erythematosus (SLE). Several studies have estimated the association between TNF-α -308 A/G and SLE risk. However, results were inconsistent. A case-control study was carried out to explore the association between TNF-α -308 A/G and the SLE risk in a Chinese Han population. Meta-analysis combining present with previous studies was conducted to further explore the association. Our case-control study included 556 patients with SLE along with 570 matched healthy controls. TNF-α -308 A allele was significantly increased in patients with SLE compared with controls (OR = 2.184, 95% CI: 1.718-2.778, P < 0.001). Genotypes AA and AG were associated with the susceptibility to SLE as compared with the GG genotype, as well as the dominant model (AA+AG versus GG), respectively. The meta-analysis included 41 comparative studies involving 4799 patients and 6635 controls. An association between SLE and allele A was found in the overall populations (OR = 1.70, 95% CI: 1.46-1.98, P < 0.001). In addition, we discussed the correlation between this polymorphism and lupus nephritis (LN) risk, showing that allele A was significantly related to LN in the overall populations (OR = 1.80, 95% CI: 1.21-2.68, P = 0.004). The results from our case-control study and the meta-analysis indicate that the TNF-α -308 A allele is significantly associated with an increased risk of SLE/LN.

The phenolic fraction of extra virgin olive oil modulates the activation and the inflammatory response of T cells from patients with systemic lupus erythematosus and healthy donors

“…TNF‐α is a proinflammatory cytokine that strongly contributes to inflammatory and immune responses by inducing a cascade of various inflammatory cytokines . Particularly, serum TNF‐α levels appeared increased in SLE patients when compared to healthy controls and they are directly correlated with SLE active disease .…”

Genetically Determined TNF-α Secretion Influences the Development of Dermatomyositis and Systemic Lupus Erythematosus

“…These results are consistent with the results reported by other authors and confi rm the functional signifi cance of the -308G/А polymorphism. 9,[13][14][15] A difference was found in the secretion of TNF-α in patients with SLE carrying the -1031TT, -1031TС, -863СС, and -863СА genotypes (р=0.009 and р=0.018, respectively). The -1031ТТ and -863СС genotypes lead to a higher secretion of TNF-α compared to the -1031ТС and -863СА genotypes.…”

TNF-α -308 G>A and IL10 -1082A>G polymorphisms as potential risk factors for lymphoproliferative disorders in autoimmune rheumatic diseases

“…The increased inflammatory activity in RA patients was significantly correlated with TNF-α concentrations in serum and synovial fluid of the patients [36,37]. Yang et al showed that TNF-α AA and AG genotypes were associated with SLE susceptibility compared with the GG genotype, and the detected increased risk of lupus nephritis was associated with -308A allele [38]. In addition, Vincent et al study showed that overexpression of the TNF family members, B cell-activating factor (BAFF) and proliferation-inducing ligand (APRIL), correlated with the increased risk of hematologic malignancies in SLE [39].…”