Tumor necrosis factor–α is a common genetic risk factor for asthma, juvenile rheumatoid arthritis, and systemic lupus erythematosus in a Mexican pediatric population

Jiménez-Morales, Silvia; Velázquez‐Cruz, Rafael; Ramírez‐Bello, Julián; Bonilla-González, Edmundo; Romero‐Hidalgo, Sandra; Escamilla-Guerrero, Guillermo; Cuevas, Francisco; Espinosa-Rosales, Francisco; Martínez-Aguilar, Nora; Gómez-Vera, Javier; Baca, Vicente; Orozco, Lorena

doi:10.1016/j.humimm.2009.01.027

Cited by 81 publications

(62 citation statements)

References 70 publications

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“…This finding is consistent with the results reported by Fuertes et al, who describe the association of an A allele of rs1800629 with an increased risk of developing allergic rhinitis in Caucasian infants [20]. In the Mexican population, Jiménez-Morales et al associated the A allele of the same SNP with asthma in pediatric patients of the female sex [21]. In the present study, this allele was not associated with risk if comparing the ATA versus HC group; however, when contrasting the AERD versus HC groups, there was an association with risk, with the GA genotype being shown to be increased in the AERD group compared with the HC group.…”

Section: Discussionsupporting

confidence: 90%

Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

et al. 2017

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Aim:To evaluate the association of three single nucleotide polymorphisms in TNF and one in LTA in Mexican patients with aspirin-exacerbated respiratory disease (AERD) and the correlation of those single nucleotide polymorphisms with serum levels of TNF-α. Patients & methods: Case-control study including 133 patients with AERD, 135 patients with asthma (aspirin-tolerant asthmatics) and 182 healthy subjects. Results: GA genotype of rs1800629 in TNF was found to be associated with the risk of developing AERD (p < 0.05; odds ratio = 2.36) and by dominant model (p < 0.05; odds ratio = 2.51). Furthermore, there was a difference in the serum levels between the aspirin-tolerant asthmatics group and the other groups (p < 0.001). Conclusion: The GA genotype of rs1800629 is associated with genetic susceptibility to AERD, but it does not correlate to protein serum levels. Aspirin-exacerbated respiratory disease (AERD) is a clinical disease characterized by hypersensitivity to aspirin, asthma and chronic rhinosinusitis with nasal polyps. It affects 10% of the population with asthma; however, its prevalence increases to 21% when provocation tests are used [1]. AERD is a disease characterized by restructuring of the airway [2] and the presence of extensive hyperplastic eosinophilic sinusitis with the formation of nasal polyps [3]. The most important clinical characteristic is bronchoconstriction after the administration of aspirin (ASA) or other nonsteroidal anti-inflammatory drugs (NSAIDs) [2,4]. The physiopathology involves a block in the cyclooxygenase pathway that promotes a diversion of arachidonic acid metabolism toward the lipoxygenase pathway, inducing the synthesis of leukotrienes such as LTC4, LTD4 and LTE4 [5,6], proteins that induce inflammatory cell chemotaxis, and the release of cytokines such as TNF-α [7] and lymphotoxin. TNF-α is a critical molecule in the regulation of inflammation because it induces a cascade of other inflammatory cytokines, chemokines and growth factors [8]. The results of various in vivo and in vitro studies indicate that the increase in their production is involved in the severity of the inflammation, due to their participation in restructuring the airway and in the pro-oxidative response [9]. In relation to single nucleotide polymorphisms (SNPs), it has been reported that rs1800629 (G→A change in position -308) increases transcriptional activity [10,11], in addition to being associated with different pulmonary pathological diseases such as chronic obstructive pulmonary disease and asthma [9,12,13]. However, no SNPs have been reported in TNF or LTA that are associated with AERD.

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Section: Discussionsupporting

confidence: 90%

Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

et al. 2017

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“…TNF2 is part of the extended haplotype HLA-A1-B8-DR3-DQ2 [14], associated with high TNF-a production [15,16] and with predisposition to several autoimmune diseases. Nevertheless, an increased risk of developing SLE, independent of the HLA-DR genotype, has been reported for carriers of TNF2 allele in Caucasian [17,18], African Americans [19], Chinese [20], North American white [21], Colombian [22] and Mexican [23] populations.…”

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor alpha promoter polymorphism −308 G/A in Brazilian patients with systemic lupus erythematosus

et al. 2012

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“…Similarly, a PTPN22 variant is common in Caucasians with RA but not in the two Asian groups. One investigation confirmed the association between the TNFA gene, specifically the TNFA -308 G/A SNP, with JIA in 725 Mexican patients under 16 years of age (171 had JIA, 226 had asthma, 328 had SLE) and 400 control subjects [47]. This finding was similar to Chilean, Iranian, and Taiwanese populations, but different from observations in Turkish, Czech, German, and Spanish populations.…”

Section: Il2ramentioning

confidence: 86%

The Genetics of Juvenile Idiopathic Arthritis: What Is New in 2010?

Angeles‐Han

Prahalad

2010

Curr Rheumatol Rep

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Juvenile idiopathic arthritis (JIA), the most common cause of chronic arthritis in children, is believed to be influenced by genetic factors. Recent studies on the genetics of JIA have not only validated proposed genetic associations but have also led to the recognition of novel genetic associations. Studies of specific genes have been modeled on the premise of shared autoimmunity, wherein genetic variants that predispose to other autoimmune phenotypes may also confer susceptibility to JIA. The advent of genome-wide association studies has accelerated the detection of non-HLA susceptibility loci in other autoimmune phenotypes and is likely to uncover novel JIA-associated variants as well. This review highlights recent genetic investigations of JIA.

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Tumor necrosis factor–α is a common genetic risk factor for asthma, juvenile rheumatoid arthritis, and systemic lupus erythematosus in a Mexican pediatric population

Cited by 81 publications

References 70 publications

Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

Tumor necrosis factor alpha promoter polymorphism −308 G/A in Brazilian patients with systemic lupus erythematosus

The Genetics of Juvenile Idiopathic Arthritis: What Is New in 2010?

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