Meta-analysis of TNF-α promoter –308A/G polymorphism and SLE susceptibility in Asian populations

Zou, Yanfeng; Feng, Xiao-Liang; Tao, Jin‐Hui; Su, Hong; Pan, Fan-Ming; Liao, Fangfang; Yu, Fan; Ye, Dong-Qing

doi:10.1007/s00296-010-1392-7

Cited by 10 publications

(5 citation statements)

References 41 publications

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“…Moreover, the role of Th1 response against L. major infection was also demonstrated in animal model of L. major [9,10]. Out of all studied Th1 cytokines, TNFα and IFN-γ were found to be critical for the initiation of preventive immunity against all studied L. species, particularly L. major [10][11][12][13]. TNF-α-308G/A polymorphism was well studied in several autoimmune/inflammatory diseases, the A allele of TNFα (308G/A) was reported to have higher transcriptional activity by 6-7 folds as compared with the common G allele [14,15].…”

Section: Introductionmentioning

confidence: 87%

TNF-α − 308 G/A and IFN-γ + 874 A/T gene polymorphisms in Saudi patients with cutaneous leishmaniasis

et al. 2020

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Background: Cutaneous leishmaniasis (CL) is well linked with immunogenetic factors. This study was undertaken to test the association of TNF-α − 308 and IFN-γ + 874 gene polymorphisms with the susceptibility of Leishmania (L) species among CL patients in central region of Saudi Arabia.Methods: This is a case-control study involved 169 Saudi subjects with different L. species and 199 healthy controls from central region of Saudi Arabia. All subjects were characterized by TNF-α − 308 G/A and IFN-γ + 874 A/T gene polymorphisms using PCR.Results: Evaluation of genotyping and allelic frequency of TNF-α − 308 G/A in different L. species showed no significant association compared to controls (p > 0.05). Except, in cases of L. tropica that showed significantly higher TNF-α − 308 A versus G allele frequency (p = 0.0004). Evaluation of genotyping of IFN-γ + 874 (TT versus AA+AT recessive) and allelic frequency of IFN-γ + 874 (T versus A) showed significant higher in L. major and also in total CL cases as compared to healthy controls (p < 0.05). Furthermore, a strong association was observed between the susceptibility of L. major, L. tropica or total CL cases with synergistically combined high TNF-α 308/INF-γ 874 alleles.Conclusions: This is the first report that shows the gene polymorphisms of TNF-α − 308 G/A and IFN-γ + 874 A/T in Saudi patients with different L. species infections. Data showed that the TNF-α-308 G/A gene polymorphism is not associated with the susceptibility of CL in Saudi subjects. The only correlation was found in between A versus G allelic frequency in L. tropica. Importantly, IFN-γ + 874 A/T polymorphism was found to be associated with the susceptibility of L. major and also with total CL subjects. Moreover, data from synergistically combined high TNF-α 308/INF-γ 874 alleles strongly suggest their potential role in the susceptibility of leishmania infection.

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Section: Introductionmentioning

confidence: 87%

TNF-α − 308 G/A and IFN-γ + 874 A/T gene polymorphisms in Saudi patients with cutaneous leishmaniasis

et al. 2020

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“…A significant genetic association between TNF-α promoter −308A/G polymorphism and SLE susceptibility in Asian populations, and in European-derived populations was detected in Zou et al (2011) and Lee et al (2006) meta-analysis respectively.…”

Section: Association Between Tnf-α Genetic Polymorphisms and Autoimmumentioning

confidence: 95%

TNF-α gene polymorphisms and expression

2016

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Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine with an important role in the pathogenesis of several diseases. Its encoding gene is located in the short arm of chromosome 6 in the major histocompatibility complex class III region. Most of the TNF-α gene polymorphisms are located in its promoter region and they are thought to affect the susceptibility and/or severity of different human diseases. This review summarizes the data related to the association between TNF-α gene and its receptor polymorphisms, and the development of autoimmune diseases. Among these polymorphisms the −308G/A TNF-α promotor polymorphism has been associated several times with the the development of autoimmune diseases, however some discrepant results have been recorded. The other TNF-α gene polymorphisms had little or no association with autoimmune diseases. Current results about the molecules controlling TNF-α expression are also presented. The discrepancy between different records could be related partly to either the differences in the ethnic origin or number of the studied individuals, or the abundance and activation of other molecules that interact with the TNF-α promotor region or other elements.

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“…TNF is a cytokine secreted by macrophages and an immunomodulatory molecule that can alter the balance of T-regulatory cells and participate in the pathogenesis of SLE [43]. Several studies have shown that TNF-α gene polymorphisms are closely related to the susceptibility to SLE [44][45][46]. IL6 is a cytokine with multiple biological functions in immunity and tissue regeneration, which is associated with the pathogenesis of SLE [47].…”

Section: Discussionmentioning

confidence: 99%

Investigating the Molecular Mechanism of Xijiao Dihuang Decoction for the Treatment of SLE Based on Network Pharmacology and Molecular Docking Analysis

Wei

Song

Gong

et al. 2022

BioMed Research International

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Objective. To elucidate the main mechanism of Xijiao Dihuang decoction (XJDHT) for the treatment of systemic lupus erythematosus (SLE). Methods. TCMSP, BATMAN-TCM, ETCM, and TCMID databases and literature search were used to screen the potential active compounds of XJDHT, and TCMSP and SwissProt databases were searched to predict the targets of the compounds. The targets of SLE were obtained from Genegards, OMIM, and DisGeNET databases, and Venn online platform was used to obtain the intersection targets of XJDHT and SLE. Afterwards, the PPI network was constructed by using the STRING database, and the core targets were identified by network topology analysis. GO and KEGG enrichment analyses were performed through R software, and molecular docking of the top three core targets and their corresponding compounds were accomplished by Autodock Vina and Pymol softwares. Results. There were 30 potential active ingredients, 289 potential targets, and 129 intersection targets screened from the above databases. Network topology analysis identified 23 core targets, such as AKT1, TNF, IL6, IL1B, and INS. GO enrichment analysis obtained 2555 terms and mainly clustering on the react to lipopolysaccharide, membrane raft, and ubiquitin-like protein ligase binding. KEGG enrichment analysis obtained 187 signaling pathways, mainly concentrating on the lipid and atherosclerosis, AGE-RAGE signaling pathway in diabetic complications, fluid shear stress, and atherosclerosis. Molecular docking verified that the active compounds of XJDHT have the strong binding activity to the core targets. Conclusion. This study preliminarily uncovers the mechanism of XJDHT acting on SLE through a “multicompound, multitarget, and multipathway” manner. XJDHT may achieve the treatment of SLE by inhibiting the proinflammatory factors, inflammatory signal cvtokines, proliferation, injury, and apoptosis processes. In summary, the present study would provide a promising theoretical basis for further clinical and experimental studies.

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Meta-analysis of TNF-α promoter –308A/G polymorphism and SLE susceptibility in Asian populations

Cited by 10 publications

References 41 publications

TNF-α − 308 G/A and IFN-γ + 874 A/T gene polymorphisms in Saudi patients with cutaneous leishmaniasis

TNF-α − 308 G/A and IFN-γ + 874 A/T gene polymorphisms in Saudi patients with cutaneous leishmaniasis

TNF-α gene polymorphisms and expression

Investigating the Molecular Mechanism of Xijiao Dihuang Decoction for the Treatment of SLE Based on Network Pharmacology and Molecular Docking Analysis

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