Are anti-nucleosome antibodies a better diagnostic marker than anti-dsDNA antibodies for systemic lupus erythematosus? A systematic review and a study of metanalysis

Bizzaro, Nicola; Villalta, Danilo; Giavarina, Davide; Tozzoli, Renato

doi:10.1016/j.autrev.2012.07.002

Cited by 123 publications

(117 citation statements)

References 46 publications

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“…However, our study did not show any correlation between antichromatin levels and lupus nephritis [53]. A recent meta-analysis of antichromatin antibody as a diagnostic marker for lupus revealed no correlation with kidney involvement [57].…”

Section: Autoantibodiescontrasting

confidence: 93%

Biomarkers for systemic lupus erythematosus: an update

Kim

Jung²,

Suh³

2015

International Journal of Clinical Rheumatology

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Section: Autoantibodiescontrasting

confidence: 93%

Biomarkers for systemic lupus erythematosus: an update

Kim

Jung²,

Suh³

2015

International Journal of Clinical Rheumatology

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“…Both anti-double-stranded DNA and antichromatin antibodies are closely associated with nephritogenicity. 2,39 Anticardiolipin IgG is commonly found in the MRL/lpr strain 40 and has been linked with proteinuria. 41 Antiribosomal P antibodies are highly specific for SLE 42 and share antigenic epitopes on the ribosome with anti-DNA antibodies.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Fibroblast Growth Factor-Inducible 14 (Fn14) Preserves the Filtration Barrier and Ameliorates Lupus Nephritis

Xia

Herlitz

Gindea

et al. 2015

Journal of the American Society of Nephrology

114

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TNF ligand superfamily member 12, also known as TNF-related weak inducer of apoptosis (TWEAK), acts through its receptor, fibroblast growth factor-inducible 14 (Fn14), to mediate several key pathologic processes involved in tissue injury relating to lupus nephritis. To explore the potential for renal protection in lupus nephritis by targeting this pathway, we introduced the Fn14 null allele into the MRL-lpr/lpr lupus mouse strain. At 26-38 weeks of age, female Fn14-knockout MRL-lpr/lpr mice had significantly lower levels of proteinuria compared with female wild-type MRL-lpr/lpr mice. Furthermore, Fn14-knockout mice had significantly improved renal histopathology accompanied by attenuated glomerular and tubulointerstitial inflammation. There was a significant reduction in glomerular Ig deposition in Fn14-knockout mice, despite no detectable differences in either serum levels of antibodies or splenic immune cell subsets. Notably, we found that the Fn14-knockout mice displayed substantial preservation of podocytes in glomeruli and that TWEAK signaling directly damaged barrier function and increased filtration through podocyte and glomerular endothelial cell monolayers. Our results show that deficiency of the Fn14 receptor significantly improves renal disease in a spontaneous lupus nephritis model through prevention of the direct injurious effects of TWEAK on the filtration barrier and/or modulation of cytokine production by resident kidney cells. Thus, blocking the TWEAK/Fn14 axis may be a novel therapeutic intervention in immune-mediated proliferative GN.

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“…Priority of anti-nucleosome immune response compared to anti-DNA and anti-histone ones is indirectly conirmed by revelation of earlier subtype of anti-nucleosome antibodies that do not interact with both DNA and histones [35]. There is close association of these antibodies with SLE activity and the kidney involvement [36]. But, unlike anti-dsDNA, anti-nucleosome antibodies do not develop glomerular deposits in the absence of nucleosomal antigens; further perfusion of nucleosome-containing ICs through the kidneys results in appearance of linear immunoglobulin deposits along glomerular basement membrane [37].…”

Section: Antibodies Induced By Immunizationmentioning

confidence: 90%

Elimination of Nucleoproteins in Systemic Lupus Erythematosus and Antinuclear Autoantibodies Production

Trofimenko¹

2017

Lupus

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The distinctive feature of systemic lupus erythematosus (SLE) is an immune reaction directed to diverse spectrum of autoantigens, which tends to change along with the disease spreading. The most common targets of the autoantibodies are protein and nucleoprotein components of cell nuclei: dsDNA, histones, nucleosomes, Sm antigen, and Ro and La antigens. Considering that the exact causes of this tolerance loss are unknown, a certain number of hypotheses are now discussed. One of the most promising is "waste disposal" concept, which makes a link between broken elimination of cellular debris, mononuclear phagocyte system dysfunction, and initiation of autoimmunity by the antigen presenting cells in SLE. This chapter concerns the ways nuclear antigens release from cells, necrosis, and apoptosis, as well as the key molecular mechanisms of transport and elimination of these antigens, its disturbances in SLE, and connection with innate immunity by mononuclear cells. Special atention is paid to nucleosomes and DNA degradation process, its principal factors (DNase I, C1q, SAP), blood DNA transportation by immune complexes, and immune stimulating action of DNA in SLE. Current pros and cons for the waste disposal concept and existing research trends in this ield are discussed.

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Are anti-nucleosome antibodies a better diagnostic marker than anti-dsDNA antibodies for systemic lupus erythematosus? A systematic review and a study of metanalysis

Cited by 123 publications

References 46 publications

Biomarkers for systemic lupus erythematosus: an update

Biomarkers for systemic lupus erythematosus: an update

Deficiency of Fibroblast Growth Factor-Inducible 14 (Fn14) Preserves the Filtration Barrier and Ameliorates Lupus Nephritis

Elimination of Nucleoproteins in Systemic Lupus Erythematosus and Antinuclear Autoantibodies Production

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