Association of the polymorphisms of TRAF1 (rs10818488) and TNFAIP3 (rs2230926) with rheumatoid arthritis and systemic lupus erythematosus and their relationship to disease activity among Egyptian patients

Moaaz, Mai; Mohannad, Nevine

doi:10.5114/ceji.2016.60991

Cited by 18 publications

(17 citation statements)

References 42 publications

(47 reference statements)

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“…SLE or SSc patients with an intron SNP (Figure 2 C) predisposes for increased risk for either renal involvement ( 132 ) or aggravated disease with fibrosing alveolitis and pulmonary hypertension ( 133 ). Similarly, RA patients with a previously described functional SNP (Figure 2 E) had more swollen joints and increased disease activity scores (DAS28) compared to RA patients without this SNP, indicating worse clinical prognosis ( 9 , 117 ). Finally, AIH patients with an upstream SNP (Figure 2 A) harbored increased liver enzymes and more cirrhosis at disease presentation compared to patients without this SNP ( 109 ).…”

Section: A20/tnfaip3 In Autoinflammatory and Autoimmune Patientsmentioning

confidence: 63%

“…NF-κB activation is tightly controlled by several mechanisms, including the key regulatory (de)ubiquitinating enzyme A20 or tumor necrosis factor α-induced protein 3 (TNFAIP3) ( 6 ). Genetic studies have demonstrated the association of TNFAIP3 single nucleotide polymorphisms (SNPs) with multiple human diseases ( 7 ), such as systemic lupus erythematosus (SLE) ( 8 – 10 ), rheumatoid arthritis (RA) ( 9 ), and Crohn’s disease (CD) ( 11 , 12 ). A20/TNFAIP3 regulates crucial stages in immune cell homeostasis, such as NF-κB activation and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

A20/Tumor Necrosis Factor α-Induced Protein 3 in Immune Cells Controls Development of Autoinflammation and Autoimmunity: Lessons from Mouse Models

Das¹,

Chen²,

Hendriks³

et al. 2018

Front. Immunol.

141

106

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Immune cell activation is a stringently regulated process, as exaggerated innate and adaptive immune responses can lead to autoinflammatory and autoimmune diseases. Perhaps the best-characterized molecular pathway promoting cell activation is the nuclear factor-κB (NF-κB) signaling pathway. Stimulation of this pathway leads to transcription of numerous pro-inflammatory and cell-survival genes. Several mechanisms tightly control NF-κB activity, including the key regulatory zinc finger (de)ubiquitinating enzyme A20/tumor necrosis factor α-induced protein 3 (TNFAIP3). Single nucleotide polymorphisms (SNPs) in the vicinity of the TNFAIP3 gene are associated with a spectrum of chronic systemic inflammatory diseases, indicative of its clinical relevance. Mice harboring targeted cell-specific deletions of the Tnfaip3 gene in innate immune cells such as macrophages spontaneously develop autoinflammatory disease. When immune cells involved in the adaptive immune response, such as dendritic cells or B-cells, are targeted for A20/TNFAIP3 deletion, mice develop spontaneous inflammation that resembles human autoimmune disease. Therefore, more knowledge on A20/TNFAIP3 function in cells of the immune system is beneficial in our understanding of autoinflammation and autoimmunity. Using the aforementioned mouse models, novel A20/TNFAIP3 functions have recently been described including control of necroptosis and inflammasome activity. In this review, we discuss the function of the A20/TNFAIP3 enzyme and its critical role in various innate and adaptive immune cells. Finally, we discuss the latest findings on TNFAIP3 SNPs in human autoinflammatory and autoimmune diseases and address that genotyping of TNFAIP3 SNPs may guide treatment decisions.

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Section: A20/tnfaip3 In Autoinflammatory and Autoimmune Patientsmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

A20/Tumor Necrosis Factor α-Induced Protein 3 in Immune Cells Controls Development of Autoinflammation and Autoimmunity: Lessons from Mouse Models

Das¹,

Chen²,

Hendriks³

et al. 2018

Front. Immunol.

141

106

View full text Add to dashboard Cite

show abstract

“…TNF‐receptor associated factor (TRAF) proteins are key adaptor molecules that play critical roles in immune cell signaling [22,23]. The TRAF1 gene encodes tumor necrosis factor (TNF) receptor associated factor 1, which is thought to be associated with a variety of TNF receptor family members [24]. By the construction of TRAF1‐pmir‐GLO and using dual‐luciferase reporter assay system, we initially confirmed that the target of miR‐483 is TRAF1.…”

Section: Discussionmentioning

confidence: 84%

Mir‐483 inhibits colon cancer cell proliferation and migration by targeting TRAF1

Niu

Jiang

et al. 2018

The Kaohsiung J of Med Scie

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MicroRNAs are important regulators during human growth and development. Emerging evidence indicates that microRNAs play important roles in colorectal cancer. The aim of this study is to reveal the biological function and direct target gene of miR-483 in colorectal cancer. The biological function of miR-483 on the proliferation and migration of colon cancer cells was then examined by Edu assay and transwell assay, respectively. Our findings revealed that miR-483 mimic could significantly inhibit cell proliferation and migration. The target gene of miR-483 was predicted by target scan software and identified by a dual fluorescence reporter system which showed that TRAF1 was a direct target gene of miR-483 in SW480 cell line. These data suggest that miR-483 is a colorectal cancer suppressor which could inhibit cell proliferation and migration, possibly via targeting TRAF1. The miR-483 could be a potential treatment target for colorectal cancer.

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“…Based on the consideration of genetic heterogeneity among different ethnic populations and possible false positive results, multiple studies have been subsequently performed to test whether the TRAF1 / C5 rs10818488 and rs3761847 polymorphisms are associated with RA in different ethnic populations [21-39]. Nevertheless, the results were inconsistent, and this discrepancy might be due to different sample sizes, genetic backgrounds, clinical heterogeneity and publication bias, etc.…”

Section: Introductionmentioning

confidence: 99%

Associations of TRAF1/C5 rs10818488 and rs3761847 polymorphisms with genetic susceptibility to rheumatoid arthritis: a case-control study and updated meta-analysis

Huang

Hua

Sun

et al. 2019

cejoi

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The results on associations of tumor necrosis factor (TNF)-receptor associated factor 1/complement component 5 (TRAF1/C5) rs10818488 and rs3761847 polymorphisms with rheumatoid arthritis (RA) are controversial, thus this study was performed to examine whether the aforementioned polymorphisms were associated with RA in a Chinese population. Furthermore, an updated meta-analysis was conducted. The polymorphisms were genotyped in 328 Chinese RA patients and 449 healthy controls. Studies examining the association of TRAF1/C5 rs10818488 and/or rs3761847 polymorphism with RA were exhaustively searched. No significant difference in either genotype or allele distribution between RA patients and controls was found. The updated meta-analysis was conducted based on 19 articles including the present study. A significant association of RA with TRAF1/C5 rs10818488 polymorphism G allele in Europeans (OR = 0.843, 95% CI = 0.730-0.975, p = 0.021) and in Asians (OR = 1.070, 95% CI = 1.009-1.136, p = 0.024) was found. Additionally, a significant association of RA with TRAF1/C5 rs10818488 polymorphism G allele under the recessive model in Asians (OR = 1.129, 95% CI = 1.023-1.246, p = 0.016) and in Africans (OR = 0.657, 95% CI = 0.507-0.851, p = 0.001) was found. Only a borderline significant association of RA with TRAF1/C5 rs3761847 polymorphism A allele was found in Europeans. Non-significant associations of RA with TRAF1/C5 rs10818488 and rs3761847 polymorphisms were found in our study. The updated meta-analysis results demonstrate that TRAF1/C5 rs10818488 polymorphism is associated with RA in Europeans, Asians and Africans, and TRAF1/C5 rs3761847 polymorphism is associated with RA in Europeans with borderline significant evidence.

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Association of the polymorphisms of TRAF1 (rs10818488) and TNFAIP3 (rs2230926) with rheumatoid arthritis and systemic lupus erythematosus and their relationship to disease activity among Egyptian patients

Cited by 18 publications

References 42 publications

A20/Tumor Necrosis Factor α-Induced Protein 3 in Immune Cells Controls Development of Autoinflammation and Autoimmunity: Lessons from Mouse Models

A20/Tumor Necrosis Factor α-Induced Protein 3 in Immune Cells Controls Development of Autoinflammation and Autoimmunity: Lessons from Mouse Models

Mir‐483 inhibits colon cancer cell proliferation and migration by targeting TRAF1

Associations of TRAF1/C5 rs10818488 and rs3761847 polymorphisms with genetic susceptibility to rheumatoid arthritis: a case-control study and updated meta-analysis

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