Serum DNase I activity in systemic lupus erythematosus: correlation with immunoserological markers, the disease activity and organ involvement

Škiljević, Dušan; Jeremić, Ivica; Nikolić, Miloš; Andrejević, Sladjana; Sefik-Bukilica, M.; Stojimirovic, Biljana; Bonaci-Nikolic, Branka

doi:10.1515/cclm-2012-0521

Cited by 45 publications

(44 citation statements)

References 16 publications

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“…Impaired degradation of chromatin by DNase1 in the process of clearance of apoptotic material is supposed to contribute to the development of SLE. In accordance with this it was shown that DNase1 activity is lower in SLE patients than in healthy individuals [39,40]. Here, we investigated DNase1 activity in the course of SLE disease progression.…”

Section: Discussionsupporting

confidence: 61%

“…In other conditions where cfDNA levels were increased, as observed after physical exercise, DNase1 activity was also elevated [32,42]. A study by Skiljevic et al found that a relapse in SLE patients is characterised by an increase of DNase1 activity but without reaching the levels of healthy individuals [40]. Therefore, we proposed a mechanism of counter regulation where enzyme activity rises in response to the rise of substrate which is, in our study, reflected by higher levels of cfDNA in blood plasma.…”

Section: Discussionmentioning

confidence: 96%

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Correlation between cell free DNA levels and medical evaluation of disease progression in systemic lupus erythematosus patients

Tug

Helmig

Menke

et al. 2014

Cellular Immunology

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 96%

Correlation between cell free DNA levels and medical evaluation of disease progression in systemic lupus erythematosus patients

Tug

Helmig

Menke

et al. 2014

Cellular Immunology

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“…Moreover, Denny et al described a distinct subset of SLE neutrophils, so-called low-density granulocytes, with increased NET releasing capabilities [23]. It has also been reported that SLE patients display a reduced NET clearance capacity due to a decreased DNase I activity and/or NET-bound C1q/ autoantibodies preventing the accessibility to the NETs of DNase I [24,25]. Both increased NETosis and reduced degradation/removal of NETs may lead to an enduring exposure of NET antigens to the immune system, thereby evoking or amplifying an anti-nuclear autoimmune response.…”

Section: Discussionmentioning

confidence: 99%

Acetylated histones contribute to the immunostimulatory potential of neutrophil extracellular traps in systemic lupus erythematosus

Pieterse

Hofstra

Berden

et al. 2014

Clinical and Experimental Immunology

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Original ArticleAcetylated histones contribute to the immunostimulatory potential of neutrophil extracellular traps in systemic lupus erythematosus OTHER ARTICLES PUBLISHED IN THIS SERIESDying autologous cells as instructors of the immune system. Clinical and Experimental Immunology 2015, 179: 1-4. Anti-dsDNA antibodies as a classification criterion and a diagnostic marker for systemic lupus erythematosus: critical remarks. Clinical and Experimental Immunology 2015, 179: 5-10. The effect of cell death in the initiation of lupus nephritis. Clinical and Experimental Immunology 2015, 179: 11-16 SummaryIn addition to disturbed apoptosis and insufficient clearance of apoptotic cells, there is recent evidence for a role of neutrophils in the aetiopathogenesis of systemic lupus erythematosus (SLE). In response to various stimuli, neutrophils can rapidly release DNA fibres decorated with citrullinated histones and anti-microbial peptides. These structures are referred to as neutrophil extracellular traps (NETs). In addition to apoptotic cell-derived microparticles, these NETs may comprise a further source of autoantigens, able to drive the autoimmune response in SLE. Our group recently identified specific histone modifications occurring during apoptosis that play an important role in the autoimmune response in SLE. In the current study, we evaluated the presence and immunostimulatory potential of these previously identified histone modifications in NETs. Compared to NETs from healthy donors, the histones present in NETs formed by SLEderived neutrophils contain increased amounts of acetylated and methylated residues, which we previously observed to be associated with apoptosis and SLE. Treatment of neutrophils with histone deacetylase (HDAC) inhibitor Trichostatin A (TSA), prior to induction of NETosis, induced NETs containing hyperacetylated histones, endowed with an increased capacity to activate macrophages. This implies that specific histone modifications, in particular acetylation, might enhance the immunostimulatory potential of NETs in SLE.

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“…Defects in expression and activity of CRP and SAP also contribute to defective clearance of necrotic cells (66, 68, 76). Some lupus patients have defective serum DNase I activity (157, 158) and they tend to have higher disease activity, and higher autoantibody levels when compared to SLE patients with normal enzyme activity (158). In mice, DNase I deficiency results in a lupus-like syndrome with glomerular immune complex deposition and glomerulonephritis (157).…”

Section: Defective Clearance Of Necrotic Cells In Lnmentioning

confidence: 99%

Cell death in the pathogenesis of systemic lupus erythematosus and lupus nephritis

Mistry

Kaplan

2017

Clinical Immunology

170

137

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Nephritis is one of the most severe complications of systemic lupus erythematosus (SLE). One key characteristic of lupus nephritis (LN) is the deposition of immune complexes containing nucleic acids and/or proteins binding to nucleic acids and autoantibodies recognizing these molecules. A variety of cell death processes are implicated in the generation and externalization of modified nuclear autoantigens and in the development of LN. Among these processes, apoptosis, primary and secondary necrosis, NETosis, necroptosis, pyroptosis, and autophagy have been proposed to play roles in tissue damage and immune dysregulation. Cell death occurs in healthy individuals during conditions of homeostasis yet autoimmunity does not develop, at least in part, because of rapid clearance of dying cells. In SLE, accelerated cell death combined with a clearance deficiency may lead to the accumulation and externalization of nuclear autoantigens and to autoantibody production. In addition, specific types of cell death may modify autoantigens and alter their immunogenicity. These modified molecules may then become novel targets of the immune system and promote autoimmune responses in predisposed hosts. In this review, we examine various cell death pathways and discuss how enhanced cell death, impaired clearance, and post-translational modifications of proteins could contribute to the development of lupus nephritis.

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Serum DNase I activity in systemic lupus erythematosus: correlation with immunoserological markers, the disease activity and organ involvement

Cited by 45 publications

References 16 publications

Correlation between cell free DNA levels and medical evaluation of disease progression in systemic lupus erythematosus patients

Correlation between cell free DNA levels and medical evaluation of disease progression in systemic lupus erythematosus patients

Acetylated histones contribute to the immunostimulatory potential of neutrophil extracellular traps in systemic lupus erythematosus

Cell death in the pathogenesis of systemic lupus erythematosus and lupus nephritis

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