Expression of T helper 17 cells and interleukin 17 in lupus nephritis patients

Saber, Nayera Z.; Maroof, Sherif H.; Soliman, Dina; Fathi, Marwa S.

doi:10.1016/j.ejr.2017.01.005

Cited by 14 publications

(11 citation statements)

References 34 publications

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“…In addition to that, urine IL‐17 level correlated significantly with proteinuria and this finding may be reflecting the higher excretion of IL‐17 that were expressed in the glomerular of LN patients as demonstrated in the previous studies . Urine IL‐17 level is suggested to be produced by the actual IL‐17 expressing T cells in kidneys and few studies found that it correlates with histological activity index grading of LN …”

Section: Discussionsupporting

confidence: 92%

“…In this study, we also found that anti‐dsDNA had positive association with higher serum and urine IL‐17A levels and this is in agreement with many other studies . IL‐17 was demonstrated to be crucial in increasing anti‐dsDNA antibody production and hence increasing the LN severity in mice .…”

Section: Discussionsupporting

confidence: 92%

“…Findings on the association or correlation of IL‐17 with disease activity in LN are more robust from previous studies . Our study findings concurred with their findings as our LN patients had significantly higher IL‐17 levels and they correlated significantly with LN activity.…”

Section: Discussionsupporting

confidence: 91%

“…Our findings concur with a few previous studies which showed a significant correlation of serum IL‐17 with SLEDAI . On the other hand, a study by Saber et al who had examined urine IL‐17 in SLE found no correlation with disease activity measured with SLEDAI. Despite significant correlation between serum and urine IL‐17A with SLEDAI and BILAG scores in our study, their sensitivity and specificity as predictors of active disease were low.…”

Section: Discussioncontrasting

confidence: 84%

“…Chen et al (2012) has studied glomerular Th17‐related cytokine expression in lupus nephritis (LN) patients and found that glomerular IL‐17 and IL‐23 expression levels were positively correlated with renal Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and histological activity index among LN patients. Later, Saber et al (2017) demonstrated that urine IL‐17 level was higher in patients with LN as compared to non‐LN patients. Therefore, our study explored the role of urine IL‐17 level as a biomarker of active LN.…”

Section: Introductionmentioning

confidence: 99%

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Serum and urine interleukin‐17A levels as biomarkers of disease activity in systemic lupus erythematosus

et al. 2019

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Objectives This study examined the correlations of both serum and urine interleukin‐17A (IL‐17A) levels with disease activity in systemic lupus erythematosus (SLE). This study was also aimed at determining their sensitivity and specificity as biomarkers of disease activity in SLE. Methods A cross‐sectional study was performed involving SLE patients (n = 120 patients) from Universiti Kebangsaan Malaysia Medical Centre (UKMMC). Serum and urinary IL‐17A levels were determined by immunoassay while disease activity was assessed using Systemic Lupus Erythematosus Disease Activity Index‐2000 (SLEDAI‐2K) and British Isles Lupus Assessment Group's 2004 index (BILAG 2004) scores. The correlations between serum and urinary IL‐17A levels with total SLEDAI‐2K and BILAG 2004 scores were determined using bivariate correlation analyses. Receiver operating characteristic curves were calculated to determine their sensitivity and specificity as disease activity biomarkers. Results Both serum and urinary IL‐17A levels correlated with total scores of BILAG 2004, BILAG renal, BILAG mucocutaneous, and SLEDAI‐2K (P < 0.05). Urine IL‐17A levels correlated positively with urine protein : creatinine index while serum IL‐17 level correlated with the BILAG hematology score (all P < 0.05). The area under curve of serum IL‐17A and urine IL‐17A with BILAG and SLEDAI scores were low (<0.75). Conclusion Despite positive correlations between serum and urine IL‐17A with SLE disease activity, both were neither sensitive nor specific as biomarkers to predict active disease. Hence, IL‐17 measurement has no role in SLE disease activity assessments and future studies are needed to search for other reliable activity biomarkers.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussioncontrasting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

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Serum and urine interleukin‐17A levels as biomarkers of disease activity in systemic lupus erythematosus

et al. 2019

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Improved Mitochondrial Metabolism and Reduced Inflammation Following Attenuation of Murine Lupus With Coenzyme Q10 Analog Idebenone

Blanco

Pedersen

Wang

et al. 2020

Arthritis & Rheumatology

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Objective A role for mitochondrial dysfunction has been proposed in the immune dysregulation and organ damage characteristic of systemic lupus erythematosus (SLE). Idebenone is a coenzyme Q10 synthetic quinone analog and an antioxidant that has been used in humans to treat diverse diseases in which mitochondrial function is impaired. This study was undertaken to assess whether idebenone ameliorates lupus in murine models. Methods Idebenone was administered orally to MRL/lpr mice at 2 different doses (1 gm/kg or 1.5 gm/kg idebenone‐containing diet) for 8 weeks. At peak disease activity, clinical, immunologic, and metabolic parameters were analyzed and compared to those in untreated mice (n = 10 per treatment group). Results were confirmed in the lupus‐prone NZM2328 mouse model. Results In MRL/lpr mice, idebenone‐treated mice showed a significant reduction in mortality incidence (P < 0.01 versus untreated mice), and the treatment attenuated several disease features, including glomerular inflammation and fibrosis (each P < 0.05 versus untreated mice), and improved renal function in association with decreased renal expression of interleukin‐17A (IL‐17A) and mature IL‐18. Levels of splenic proinflammatory cytokines and inflammasome‐related genes were significantly decreased (at least P < 0.05 and some with higher significance) in mice treated with idebenone, while no obvious drug toxicity was observed. Idebenone inhibited neutrophil extracellular trap formation in neutrophils from lupus‐prone mice (P < 0.05) and human patients with SLE. Idebenone also improved mitochondrial metabolism (30% increase in basal respiration and ATP production), reduced the extent of heart lipid peroxidation (by one‐half that of untreated mice), and significantly improved endothelium‐dependent vasorelaxation (P < 0.001). NZM2328 mice exposed to idebenone also displayed improvements in renal and systemic inflammation, reducing the kidney pathology score (P < 0.05), IgG/C3 deposition (P < 0.05), and the gene expression of interferon, proinflammatory, and inflammasome‐related genes (at least P < 0.05 and some with higher significance). Conclusion Idebenone ameliorates murine lupus disease activity and the severity of organ damage, supporting the hypothesis that agents that modulate mitochondrial biologic processes may have a therapeutic role in human SLE.

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The star target in SLE: IL-17

Yang

Chen

et al. 2022

Inflamm. Res.

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Expression of T helper 17 cells and interleukin 17 in lupus nephritis patients

Cited by 14 publications

References 34 publications

Serum and urine interleukin‐17A levels as biomarkers of disease activity in systemic lupus erythematosus

Serum and urine interleukin‐17A levels as biomarkers of disease activity in systemic lupus erythematosus

Improved Mitochondrial Metabolism and Reduced Inflammation Following Attenuation of Murine Lupus With Coenzyme Q10 Analog Idebenone

The star target in SLE: IL-17

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