Urinary B-cell-activating factor of the tumour necrosis factor family (BAFF) in systemic lupus erythematosus

Vincent, Fabien B.; Kandane‐Rathnayake, Rangi; Hoi, Alberta; Slavin, Laura; Godsell, Jack; Kitching, A. Richard; Harris, James; Nelson, Christina; Jenkins, Alicia J.; Chrysostomou, Anastasia; Hibbs, Margaret L.; Kerr, Peter G.; Rischmueller, Maureen; Mackay, Fabienne; Morand, Eric Francis

doi:10.1177/0961203318804885

Cited by 17 publications

(12 citation statements)

References 33 publications

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“…Therefore, it is necessary to identify non-invasive biomarkers that can be easily obtained and reflect current renal inflammation [ 34 ]. Over the last two decades, many clinical studies have demonstrated the presence of molecules associated with B-cell activation in the serum [ 29 , [35] , [36] , [37] ] and kidney tissues [ 24 , 26 , 28 , 38 ] of active LN patients. One study demonstrated that serum BAFF level was lower in SLE patients with nephrotic-range proteinuria than in SLE patients with less severe proteinuria.…”

Section: Discussionmentioning

confidence: 99%

“…Like BAFF, APRIL has been investigated as a non-invasive prognostic biomarker for severe LN [ 29 ]. Expression levels of APRIL mRNA were significantly higher in glomeruli and the tubulointerstitial compartment of biopsy samples from patients with proliferative LN compared to controls as measured by real-time PCR [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several animal model studies have demonstrated pathogenic roles for BAFF, APRIL, and their receptors in SLE and LN, and human clinical studies have demonstrated immunohistochemical expression of BAFF in glomeruli and tubular epithelial cells [ [24] , [25] , [26] , [27] , [28] , [29] ]. However, there are many obvious advantages of urinary detection.…”

Section: Introductionmentioning

confidence: 99%

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Expression of BAFF, APRIL, and cognate receptor genes in lupus nephritis and potential use as urinary biomarkers

Aguirre-Valencia

Ríos-Serna

Posso-Osorio

et al. 2020

Journal of Translational Autoimmunity

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Background B-cell activating factor (BAFF), a proliferation-inducing ligand (APRIL), and their receptors BAFF-R, BCMA, and TACI are crucial factors for the survival of B lymphocytes. Recent evidence has also demonstrated the importance of BAFF/APRIL signaling in lupus nephritis (LN). This study evaluated the relationships between LN clinical characteristics and the urinary expression levels of BAFF, APRIL, and cognate receptors to assess their potential value as disease biomarkers. Methods Expression levels of these genes were assessed in urine samples collected from systemic lupus erythematosus (SLE) patients before renal biopsy using reverse transcription real-time PCR. Results Thirty-five patients with LN were included. Most of the patients were female (82.86%) with median Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) of 15. BAFF mRNA was detectable in 28.57%, APRIL mRNA in 42.85%, BR3 mRNA in 48.57%, and TACI mRNA in 42.85% of urine samples. On the other hand, urinary (u)BCMA mRNA was not found in any sample. Urinary expression of most biomarkers was detected with greater frequency in class III and IV LN compared to class V LN. The expression level of uBR3 mRNA was correlated with SLEDAI-2K and histological activity index. Conclusion Urinary expression of BAFF/APRIL signaling factors, especially TACI, APRIL, and BR3 mRNAs, may be useful biomarkers for LN.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Expression of BAFF, APRIL, and cognate receptor genes in lupus nephritis and potential use as urinary biomarkers

Aguirre-Valencia

Ríos-Serna

Posso-Osorio

et al. 2020

Journal of Translational Autoimmunity

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“…TNFSF13B is also known as a lymphocyte B stimulator or B-cell activating factor (BAFF), in reference to its involvement in the activation, proliferation, and differentiation of this type of cell [15]. The impairment of TNFSF13B has been described in autoimmune diseases such as systemic lupus erythematosus [17], Sjögren syndrome [17, 18], and especially, rheumatic diseases [19], although always with significantly higher levels than the healthy controls. BAFF (TNFSF13B) is defined as a function regulator of B and T cells, with proinflammatory and anti-inflammatory effects [15, 18].…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of Inflammation-Related Genes in Down Syndrome Patients with or without Periodontal Disease

Baus-Domínguez

Gómez-Díaz

Torrés-Lagares

et al. 2019

Mediators of Inflammation

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Aim Aware that Down Syndrome patients present among their clinical characteristics impaired immunity, the aim of this study is to identify the statistically significant differences in inflammation-related gene expression by comparing Down Syndrome patients with Periodontal Disease (DS+PD+) with Down Syndrome patients without Periodontal Disease (DS+PD-), and their relationship with periodontitis as a chronic oral inflammatory clinical feature. Materials and Methods Case study and controls on eleven Down Syndrome patients (DS+PD+ vs. DS+PD-). RNA was extracted from peripheral blood using a Qiagen PAXgene Blood miRNA Kit when performing an oral examination. A search for candidate genes (92 selected) was undertaken on the total genes obtained using a Scientific GeneChip® Scanner 3000 (Thermo Fisher Scientific) and Clariom S solutions for human, mouse, and rat chips, with more than 20,000 genes annotated for measuring expression levels. Results Of the 92 inflammation-related genes taken initially, four genes showed a differential expression across both groups with a p value of <0.05 from the data obtained using RNA processing of the patient sample. Said genes were TNFSF13B (p = 0.0448), ITGB2 (p = 0.0033), ANXA3 (p = 0.0479), and ANXA5 (p = 0.016). Conclusions There are differences in inflammation-related gene expression in Down Syndrome patients when comparing patients who present a state of chronic oral inflammation with patients with negative rates of periodontal disease.

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“…Awareness of the steroid-sparing effects of belimumab may have contributed to rapid tapering of glucocorticoid doses, which in turn unveiled renal activity. Belimumab binds to the soluble counterpart of BAFF, a molecule implicated in the pathogenesis of LN [ 20 , 21 ], and has been shown to alter absolute and relative numbers of B cell subsets, mainly B cells of early developmental stages [ 22 , 23 ]. However, the long-term consequences of BAFF inhibition, e.g.…”

Section: Discussionmentioning

confidence: 99%

De novo lupus nephritis during treatment with belimumab

et al. 2020

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Objective In light of reports of de novo LN during belimumab (BLM) treatment, we sought to determine its frequency and contributing or protective factors in a real-life setting. Methods Patients with SLE who received BLM between 2011 and 2017 at five European academic practices were enrolled (n = 95) and followed longitudinally for a median time of 13.1 months [interquartile range (IQR): 6.0–34.7]; 52.6% were anti-dsDNA positive, 60.0% had low complement levels, and 69.5% had no renal involvement prior to/at BLM initiation [mean disease duration at baseline: 11.4 (9.3) years]. Age- and sex-matched patients with non-renal SLE who had similar serological profiles, but were not exposed to BLM, served as controls (median follow-up: 132.0 months; IQR: 98.3–151.2). Results We observed 6/66 cases (9.1%) of biopsy-proven de novo LN (4/6 proliferative) among the non-renal BLM-treated SLE cases after a follow-up of 7.4 months (IQR: 2.7–22.2). Among controls, 2/66 cases (3.0%) of de novo LN (both proliferative) were observed after 21 and 50 months. BLM treatment was associated with an increased frequency and/or shorter time to de novo LN [hazard ratio (HR): 10.7; 95% CI: 1.7, 67.9; P = 0.012], while concomitant use of antimalarial agents along with BLM showed an opposing association (HR: 0.2; 95% CI: 0.03, 0.97; P = 0.046). Conclusion Addition of BLM to standard-of-care did not prevent LN in patients with active non-renal SLE, but a favourable effect of concomitant use of antimalarials was implicated. Studies of whether effects of B-cell activating factor inhibition on lymphocyte subsets contribute to LN susceptibility are warranted.

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Urinary B-cell-activating factor of the tumour necrosis factor family (BAFF) in systemic lupus erythematosus

Cited by 17 publications

References 33 publications

Expression of BAFF, APRIL, and cognate receptor genes in lupus nephritis and potential use as urinary biomarkers

Expression of BAFF, APRIL, and cognate receptor genes in lupus nephritis and potential use as urinary biomarkers

Differential Expression of Inflammation-Related Genes in Down Syndrome Patients with or without Periodontal Disease

De novo lupus nephritis during treatment with belimumab

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