Association of the interleukin-6 polymorphisms with systemic lupus erythematosus: a meta-analysis

Cui, Yiyao; Fu, Chaowei; Jiang, Feng; Ye, L X; Wang, Meng

doi:10.1177/0961203315588971

Cited by 28 publications

(23 citation statements)

References 33 publications

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“…Data showed that the miR‐410 level in kidney tissue of MRL/lpr mice was twice lower than that in BALB/C mice (1.00 ± 0.00 in BALB/C mice vs 0.52 ± 0.11 in MRL/lpr mice, ** P < 0.01). Also it was reported that IL‐6 was an important pro‐inflammatory cytokine, which played a potential pathological role in SLE . Then, the IL‐6 levels in serum of MRL/lpr and BALB/C mice were tested using enzyme‐linked immunosorbent assay (ELISA) analysis, and data showed that the serum level of IL‐6 between BALB/C and MRL/lpr mice was 35.39 ± 12.01 versus 172.22 ± 65.66 (** P < 0.01, Fig.…”

Section: Resultsmentioning

confidence: 92%

“…Also it was reported that IL-6 was an important pro-inflammatory cytokine, which played a potential pathological role in SLE. 17 Then, the IL-6 levels in serum of MRL/lpr and BALB/C mice were tested using enzyme-linked immunosorbent assay (ELISA) analysis, and data showed that the serum level of IL-6 between BALB/C and MRL/ lpr mice was 35.39 AE 12.01 versus 172.22 AE 65.66 (**P < 0.01, Fig. 2c).…”

Section: Resultsmentioning

confidence: 99%

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miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis

Zhang

et al. 2016

Clin Exp Pharma Physio

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Lupus nephritis (LN) is a highly complex autoimmune disease caused by systemic lupus erythematosus (SLE). MicroRNAs (miRNAs) play a vital role in the pathogenesis of SLE. Previously, a total of 29 miRNAs were identified to be down-regulated in SLE patients, in which miR-410 was likely to be involved in the signalling transduction pathways in regulating the pathogenesis of SLE. The purpose of this study was to investigate the role of miR-410 in LN and to find out whether miR-410 regulates the expression of interleukin (IL)-6 and fibrosis in LN. It was found that the expression level of miR-410 in kidney tissue of MRL/lpr mice was decreased compared to that in BALB/C mice, whereas the level of IL-6 was overexpressed in MRL/lpr mice. Luciferase assay showed that miR-410 binds directly to the 3' untranslated region (UTR) of IL-6, with the results showing that overexpression of miR-410 significantly decreased the expression level of IL-6 in SV40MES13 cells. Moreover, overexpression of miR-410 significantly reduced the expression levels of fibrosis factors such as transforming growth factor-β1 (TGF-β1) and collagen I/III in SV40MES13 cells; Inhibition of the expression of miR-410 with miR-410 inhibitor resulted in increased levels of IL-6 as well as fibrosis factors. The results identify that miR-410, as a novel and critical factor in the pathogenesis of LN, decreases IL-6 expression by binding directly to the 3'UTR and suppresses fibrosis through down-regulation of TGF-β1 in SV40MES13 cells. Our study brings new insight into understanding the complex mechanisms involved in the pathogenesis of lupus disease.

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Section: Resultsmentioning

confidence: 92%

Section: Resultsmentioning

confidence: 99%

miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis

Zhang

et al. 2016

Clin Exp Pharma Physio

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“…In addition, interleukin- (IL-) 6 is a key cytokine that inhibits Foxp3 expression during Treg cell differentiation [24]. Previous studies have demonstrated that hyperoxia-induced stress and oxidative damage lead to an increase in IL-6, and, concordantly, increased production of IL-6 has been documented in SLE patients [24, 25]. Thus, oxidative stress-induced increased production of IL-6 may be the primary reason for the decrease in Treg cells in SLE patients.…”

Section: Oxidative Stress and Treg Cellsmentioning

confidence: 99%

Oxidative Stress and Treg and Th17 Dysfunction in Systemic Lupus Erythematosus

Yang

Zou

et al. 2016

Oxidative Medicine and Cellular Longevity

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Systemic lupus erythematosus (SLE) is an autoimmune disease that involves multiple organ systems. The pathogenic mechanisms that cause SLE remain unclear; however, it is well recognized that the immune balance is disturbed and that this imbalance contributes to the autoimmune symptoms of SLE. Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and the ability of the biological system to readily detoxify the reactive intermediates or to repair the resulting damage. In humans, oxidative stress is involved in many diseases, including atherosclerosis, myocardial infarction, and autoimmune diseases. Numerous studies have confirmed that oxidative stress plays an important role in the pathogenesis of SLE. This review mainly focuses on the recent research advances with respect to oxidative stress and regulatory T (Treg)/helper T 17 (Th17) cell dysfunction in the pathogenesis of SLE.

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“…9 Previous studies have implicated IL-6 polymorphisms in some inflammatory diseases such as systemic lupus erythematosus and rheumatoid arthritis. 10,11 In a Pakistani study, the GG variant genotype of the IL-6 572 SNP had its highest expression in the healthy population, whereas other genotypic variants (GC+CC) had high expression in patients with acne. In addition, IL-6 572 G allele was shown to have a protective role against acne in a Pakistani population and periodontitis in a European population.…”

Section: Introductionmentioning

confidence: 98%

Association of interleukin‐6 gene promoter polymorphism with acne vulgaris and its severity

et al. 2019

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Background. Acne vulgaris (AV) is an inflammatory disorder with a possible genetic background. Different cytokines and mediators are involved in its pathogenesis. Aim. Our aim was to investigate the interleukin (IL)-6 572 polymorphism in patients with AV and its relation to patient sex and acne severity. Methods. In total, 30 patients with acne and 20 healthy controls (HCs) were enrolled. The Global Acne Grading System was used to assess acne severity. The IL-6 572 gene promoter polymorphism was assessed using the PCR-restriction fragment length polymorphism method.Results. There was a significantly higher association of IL-6 572 variants genotypes in patients with acne (93%) compared with the HC group (45%) (P < 0.001), with a higher incidence of the IL-6 572 CC polymorphism in patients with acne. A significant difference (P < 0.001) between C and G alleles in patients vs. HCs was detected. There were no significant associations between the IL-6 572 variant genotypes and either patient sex or AV severity. Conclusion. IL-6 gene promoter polymorphism might have a role in AV susceptibility but it is not related to AV severity.

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Association of the interleukin-6 polymorphisms with systemic lupus erythematosus: a meta-analysis

Abstract: This meta-analysis provides evidence of the association between the IL-6 polymorphism and the risk of SLE, hinting that the IL-6-174 G/C and IL-6-572 G/C polymorphisms may play a role in SLE susceptibility.

Cited by 28 publications

References 33 publications

miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis

miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis

Oxidative Stress and Treg and Th17 Dysfunction in Systemic Lupus Erythematosus

Association of interleukin‐6 gene promoter polymorphism with acne vulgaris and its severity

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