Association of interleukin 13 gene polymorphisms and plasma IL 13 level with risk of systemic lupus erythematosus

Wang, Rong; Lu, Yulan; Huang, Hua‐Tuo; Qin, Haimei; Yan, Liang; Wang, Junli; Wang, Chunfang; Wei, Ye‐Sheng

doi:10.1016/j.cyto.2017.09.034

Cited by 12 publications

(10 citation statements)

References 38 publications

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“…The key DAGs contributing to this cluster included B2M, IGHG3, IL7R, ETS1, RPS19, and TNFAIP3. The pathway enrichment for the SLE DIME network includes pathways that are heavily described in the literature for SLE, such as the neutrophil degranulation pathways or NETosis 37–41 , interleukin 4 and interleukin 13 signaling 42,43 , TLR signaling pathway 44 , translocation of ZAP70 to immunological synapsis 45 , and immune-regulatory interactions between lymphoid and non-lymphoid cells ( Supplementary Figure 4A ).…”

Section: Resultsmentioning

confidence: 99%

Integration of immunome with disease-gene network reveals common cellular mechanisms between IMIDs and drug repurposing strategies

Devaprasad

Pandit

2019

Preprint

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Section: Resultsmentioning

confidence: 99%

Integration of immunome with disease-gene network reveals common cellular mechanisms between IMIDs and drug repurposing strategies

Devaprasad

Pandit

2019

Preprint

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“…Furthermore, IL-4 can downregulate T h 1-mediated IgG subclasses of autoantibodies to prevent the development of lupus-like autoimmune disease ( 22 ). Although IL-13 is a strong anti-inflammatory cytokine that modulates macrophages, monocytes, and lymphocytes ( 23 ), a previous study found that plasma IL-13 levels were significantly higher in SLE patients than in controls ( 24 ). We hypothesize that different stages and timing are key factors governing the IL-13 concentration.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, a disproportionate increase in IFN-γ or reduced IL-13 could be the mechanism in SLE. These differences could be due to possible feedback mechanism in vivo ( 24 ), which needs to be investigated by further or future studies. Alternatively, this could be due to different evolution—primary SLE and drug-induced SLE (TAILS).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Tumor Necrosis Factor-Alpha Inhibitor-Induced Systemic Lupus Erythematosus

Yen

Chen

et al. 2022

Front. Med.

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Systemic lupus erythematosus induced by biologics mainly results from tumor necrosis factor-alpha remains unclear. The objectives of the study were to investigate the mechanisms of tumor necrosis factor-alpha inhibitor-induced systemic lupus erythematosus. Peripheral blood mononuclear cells obtained from thirteen psoriasis patients were cultured and treated with the following: untreated control, Streptococcus pyogenes with or without different biologics. The supernatants were collected for cytokines assay. Analysis of cytokine expression revealed that IL-2 and IL-10 levels decreased only in the TNF-α inhibitor-treated groups but not in the groups treated with biologics involving IL-17, IL-12/IL-23 or IL-23 inhibitor mechanisms (p < 0.001, p < 0.05). The IFN-γ/IL-13 ratio increased significantly in patients with SLE inducing biologics to S. pyogenes induction only compared with non-SLE inducing biologics to S. pyogenes induction only (p = 0.001). IL-2 and IL-10 depletion and a shift to the Th-1 pathway in the innate response are the correlated mechanism for tumor necrosis factor-alpha inhibitor-induced systemic lupus erythematosus.

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“…The burden of SLE is not only physical and mental health but also socioeconomic impact because the most common age of onset is 20-40 years, and patients with that age are still raising or supporting families [2]. Risk factors of SLE included cigarette smoking, oxidative stress, ultraviolet light, infection, and hormonal action as well as genetic factors [3][4][5][6][7][8][9][10][11][12]. Environmental exposure may trigger SLE in individuals who carry a predisposing background of genetic susceptibility [2,4,7].…”

Section: Introductionmentioning

confidence: 99%

“…Environmental exposure may trigger SLE in individuals who carry a predisposing background of genetic susceptibility [2,4,7]. Several single-nucleotide polymorphisms (SNPs) in coding genes have been found to be involved in the pathogenesis of SLE, such as rs1051169 in S100B [8]; rs20541 in interleukin-(IL-) 13 [9]; rs11556218, rs4778889, and rs4072111 in IL-16 [10]; rs2227513 in IL-22 [11]; and rs7977932 in IL-31 [12].…”

Section: Introductionmentioning

confidence: 99%

Interaction of miR-181b and IFNA1 Polymorphisms on the Risk of Systemic Lupus Erythematosus

Yang

Zeng

Shi

2020

BioMed Research International

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Introduction. A previous work has discovered that chromosome 1q32 locus linked to the risk of systemic lupus erythematosus (SLE) and miR-181b located on the susceptibility site with downregulation inversely correlating to its target molecular interferon alpha 1 (IFNA1). The purpose of this study was to investigate the association of miR-181b and IFNA1 polymorphisms with IS risk. Methods. The miR-181b rs322931, IFNA1 rs1332190, and rs10811543 were genotyped using a Multiplex SNaPshot assay. miR-181b expression levels in plasma of SLE patients and controls were analyzed using quantitative PCR. Results. The rs322931 CT, CT/TT, and T allele exerted an increased trend of SLE risk (CT vs. CC: adjusted OR=1.71, 95% CI 1.16-2.50, P=0.01; CT/TT vs. CC: adjusted OR=1.45, 95% CI 1.08-1.95, P=0.01; T vs. C: adjusted OR=1.38, 95% CI 1.07-1.79, P=0.01). Combined genotypes of the rs322931 CT/TT+rs1332190 TT and the rs322931 CC+rs10811543 AG/AA also revealed an increased risk of SLE. Gene-gene interaction analysis showed that a three-locus model consisting of rs322931, rs1332190, and rs10811543 attributed an increased risk of SLE. Further genotype-phenotype analysis revealed that rs322931 CT/TT carriers displayed lower levels of miR-181b. Conclusions. These findings indicate that the miR-181b rs322931 may be singly and jointly responsible for the etiology of SLE by altering miR-181b expression.

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Association of interleukin 13 gene polymorphisms and plasma IL 13 level with risk of systemic lupus erythematosus

Cited by 12 publications

References 38 publications

Integration of immunome with disease-gene network reveals common cellular mechanisms between IMIDs and drug repurposing strategies

Integration of immunome with disease-gene network reveals common cellular mechanisms between IMIDs and drug repurposing strategies

Mechanisms of Tumor Necrosis Factor-Alpha Inhibitor-Induced Systemic Lupus Erythematosus

Interaction of miR-181b and IFNA1 Polymorphisms on the Risk of Systemic Lupus Erythematosus

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