Tumor necrosis factor gene polymorphisms are associated with systemic lupus erythematosus susceptibility or lupus nephritis in Mexican patients

Ramírez‐Bello, Julián; Cadena-Sandoval, Daniel; Mendoza-Rincón, Jorge Flavio; Barbosa-Cobos, Rosa Elda; Sánchez‐Muñoz, Fausto; Amezcua-Guerra, Luís M.; Sierra-Martínez, Mónica; Jiménez-Morales, Silvia

doi:10.1007/s12026-018-8993-8

Cited by 15 publications

(11 citation statements)

References 33 publications

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“…Genetic studies have revealed that gene polymorphisms of TNF-α are risk factors for the development of nephrotic syndrome among Egyptian children and are linked with steroid resistance [79]. Additionally, some TNF gene polymorphisms in Mexican patients were associated with systemic lupus erythematosus (SLE) and lupus nephritis [80].…”

Section: Tumor Necrosis Factormentioning

confidence: 99%

Review on Inflammation Markers in Chronic Kidney Disease

et al. 2021

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Chronic kidney disease (CKD) is one of the major health problems of the modern age. It represents an important public health challenge with an ever-lasting rising prevalence, which reached almost 700 million by the year 2017. Therefore, it is very important to identify patients at risk for CKD development and discover risk factors that cause the progression of the disease. Several studies have tackled this conundrum in recent years, novel markers have been identified, and new insights into the pathogenesis of CKD have been gained. This review summarizes the evidence on markers of inflammation and their role in the development and progression of CKD. It will focus primarily on cytokines, chemokines, and cell adhesion molecules. Nevertheless, further large, multicenter studies are needed to establish the role of these markers and confirm possible treatment options in everyday clinical practice.

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Section: Tumor Necrosis Factormentioning

confidence: 99%

Review on Inflammation Markers in Chronic Kidney Disease

et al. 2021

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“…TNF-α is coded and regulated by TNF-α gene, which is located in chromosome 6, within the class III region of MHC (9). Several studies analyzed the association of TNF-α gene with susceptibility to RA and SLE (10 –12) and numbers of single-nucleotide polymorphisms (SNPs) of TNF-α gene were identified. Among these, two common polymorphisms in the promoter, G to A substitution at position -238 ( TNF-α-238G/A, rs361525) and position -308 ( TNF-α-308G/A, rs1800629), attracted widespread attention.…”

Section: Introductionmentioning

confidence: 99%

Association between tumor necrosis factor polymorphisms and rheumatoid arthritis as well as systemic lupus erythematosus: a meta-analysis

Chen

Huang

Liao

et al. 2019

Braz J Med Biol Res

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Tumor necrosis factor-alpha ( TNF-α ) plays an important role in autoimmune diseases. Previous studies have investigated the association of TNF-α-238G/A (rs361525) and -308G/A (rs1800629) polymorphisms with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). However, no agreed conclusion had been made. Therefore, this meta-analysis was conducted to assess the associations of TNF-α-238G/A and -308G/A polymorphisms with RA and SLE risk. A systematic search was conducted in commonly used databases. Meta-analysis was performed by STATA12.0. A total of 43 studies were included. In the overall population, the TNF-α-238A allele was observed to be a protective factor for RA (A vs G: OR=0.75, 95%CI=0.57–0.99, P=0.040) and the TNF-α-308A allele was found to be a risk factor for SLE (A vs G: OR=1.78, 95%CI=1.45–2.19, P<0.001). However, no evidence of association was found between TNF-α -238 G/A polymorphism and SLE nor between -308G/A and RA. In the subgroup analysis, TNF-α-308A allele played a pathogenic role for RA in Latin Americans (A vs G: OR=1.46, 95%CI=1.15–1.84, P=0.002) and for SLE in Latin Americans (A vs G: OR=2.12, 95%CI=1.32–3.41, P=0.002) and Europeans (A vs G: OR=2.03, 95%CI=1.56–2.63, P<0.001), while it played a protective role for RA in Asians (A vs G: OR=0.54, 95%CI=0.32–0.90, P=0.017). No significant association was found between TNF-α-308G/A and SLE susceptibility in Africans and Asians. This meta-analysis demonstrated that TNF-α-238A was associated with decreased risk of RA rather than SLE, while -308G/A polymorphism was associated with SLE rather than RA. Stratification analysis indicated that different ethnicities would have different risk alleles.

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“…Models have been developed to confirm the susceptibility conferred by genes in the MHC III region (non-classical HLA and non-HLA genes) linked to HLA-B and -DRB1. The most important linked genes using HLA-DRB1 ∗ 03:01 as covariant are: the proto-oncogene Notch homologue 4 (NOTCH4), the MHC class I polypeptide–related sequence A and B (MIC-A and MIC-B), the steroid 21-hydroxylase (CYP21A2), ( Partanen et al, 1988 ; Morris et al, 2012 ) the three 70 kDa heat-shock proteins (HSPA1A, HSPA1B, HSPA1L), ( Mišunová et al, 2017 ), natural cytotoxicity triggering receptor 3 (NCR3); nuclear factor kappa light chain gene enhancer in B cells inhibitor-like 1 (NFKBIL1), allograft inflammatory factor 1 (AIF1) ( Dorak et al, 2006 ); and the three Tumor Necrosis Factor genes (Lymphotoxin-beta, Lymphotoxin-alpha, and TNF-α) ( Zúñiga et al, 2001 ; Ramírez-Bello et al, 2018 ). Important variants of the genes mentioned above have been deeply studied in Caucasians, and linkage disequilibrium with HLA-B ∗ 08:01 and -DRB1 ∗ 03:01 has been confirmed ( Dorak et al, 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Heterogeneity of Genetic Admixture Determines SLE Susceptibility in Mexican

et al. 2021

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Systemic Lupus Erythematosus (SLE) is an autoimmune inflammatory disorder for which Major Histocompatibility Complex (MHC) genes are well identified as risk factors. SLE patients present different clinical phenotypes, which are partly explained by admixture patterns variation among Mexicans. Population genetic has insight into the high genetic variability of Mexicans, mainly described through HLA gene studies with anthropological and biomedical importance. A prospective, case-control study was performed. In this study, we recruited 146 SLE patients, and 234 healthy individuals were included as a control group; both groups were admixed Mexicans from Mexico City. The HLA typing methods were based on Next Generation Sequencing and Sequence-Based Typing (SBT). The data analysis was performed with population genetic programs and statistical packages. The admixture estimations based on HLA-B and -DRB1 revealed that SLE patients have a higher Southwestern European ancestry proportion (48 ± 8%) than healthy individuals (30 ± 7%). In contrast, Mexican Native American components are diminished in SLE patients (44 ± 1%) and augmented in Healthy individuals (63 ± 4%). HLA alleles and haplotypes’ frequency analysis found variants previously described in SLE patients from Mexico City. Moreover, a conserved extended haplotype that confers risk to develop SLE was found, the HLA-A∗29:02∼C∗16:01∼B∗44:03∼DRB1∗07:01∼DQB1∗02:02, pC = 0.02, OR = 1.41. Consistent with the admixture estimations, the origin of all risk alleles and haplotypes found in this study are European, while the protection alleles are Mexican Native American. The analysis of genetic distances supported that the SLE patient group is closer to the Southwestern European parental populace and farthest from Mexican Native Americans than healthy individuals. Heterogeneity of genetic admixture determines SLE susceptibility and protection in Mexicans. HLA sequencing is helpful to determine susceptibility alleles and haplotypes restricted to some populations.

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Tumor necrosis factor gene polymorphisms are associated with systemic lupus erythematosus susceptibility or lupus nephritis in Mexican patients

Cited by 15 publications

References 33 publications

Review on Inflammation Markers in Chronic Kidney Disease

Review on Inflammation Markers in Chronic Kidney Disease

Association between tumor necrosis factor polymorphisms and rheumatoid arthritis as well as systemic lupus erythematosus: a meta-analysis

Heterogeneity of Genetic Admixture Determines SLE Susceptibility in Mexican

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