Antineutrophil cytoplasmic antibodies in patients with systemic lupus erythematosus: prevalence, antigen specificity, and clinical associations

Manolova, Irena; Dancheva, M.; Halacheva, Krasimira

doi:10.1007/s002960100108

Cited by 54 publications

(17 citation statements)

References 30 publications

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“…Manolova et al found that ANCA were associated with the particular clinical features of SLE and correlated with disease activity. 13 Pradhan et al also reported that ANCA was positively associated with SLE disease activity, and might be used as a potential complementary parameter to differentiate lupus nephritis from SLE without nephritis. 14 On the contrary, others reported no link.…”

Section: Discussionmentioning

confidence: 99%

Anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus

Xiao

Yang

et al. 2017

An. Bras. Dermatol.

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BackgroundThe clinical significance of anti-neutrophil cytoplasmic antibodies in patients with new-onset systemic lupus erythematosus, especially in systemic disease accompanied by interstitial lung disease remains to be elucidated.ObjectivesThis study was designed to investigate the role of anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus patients.MethodsA hundred and seven patients with new-onset SLE were enrolled. Presence of anti-neutrophil cytoplasmic antibodies in the sera was assessed by indirect immunofluorescence as well as enzyme linked immunosorbent assay against proteinase-3 and myeloperoxidase. Clinical features and laboratory parameters of patients were also recorded. All patients were subjected to chest X-ray, chest high-resolution computed tomography and pulmonary function test.ResultsForty-five systemic lupus erythematosus patients (45/107, 42%) were seropositive for anti-neutrophil cytoplasmic antibodies. Compared with anti-neutrophil cytoplasmic antibodies-negative patients, the anti-neutrophil cytoplasmic antibodies-positive patients had significantly higher incidence of renal involvement, anemia, and Raynaud's phenomenon as well as decreased serum level of complement 3/complement 4 and elevated erythrocyte sedimentation rate. In addition, there was a positive correlation between serum anti-neutrophil cytoplasmic antibodies level and disease activity of systemic lupus erythematosus. Furthermore, prevalence of interstitial lung disease in the anti-neutrophil cytoplasmic antibodies -positive patients (25/45, 55.6%) was obviously higher than that in the anti-neutrophil cytoplasmic antibodies-negative patients (15/62, 24.2%).Study limitationsThe sample size was limited and the criteria for screening new-onset systemic lupus erythematosus patients might produce bias.ConclusionsThe level of anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus patients correlates positively with the disease activity and the prevalence of interstitial lung disease.

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Section: Discussionmentioning

confidence: 99%

Anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus

Xiao

Yang

et al. 2017

An. Bras. Dermatol.

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“…MPO and PR3 were subsequently identified as the predominant autoantigens in 1988 and 1990, respectively (Falk and Jennette, 1988; Ludemann et al, 1990). Anti-neutrophil autoantibodies (not necessarily targeting MPO and PR3) have also been described in SS and SLE (Lamour et al, 1995; Manolova et al, 2001), with recent evidence that neutrophil antimicrobial peptides are among the antigens targeted in SLE (Lande et al, 2011). It is also important to note that neutrophils express high levels of peptidylarginine deiminase enzymes (PAD2 and PAD4; Darrah et al, 2012), which are responsible for generating citrullinated proteins, currently the most specific targets of the immune response defined in RA (Wegner et al, 2010).…”

Section: Neutrophils In Systemic Autoimmune Diseasesmentioning

confidence: 99%

NETs: the missing link between cell death and systemic autoimmune diseases?

Darrah¹,

Andrade²

2013

Front. Immun.

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For almost 20 years, apoptosis and secondary necrosis have been considered the major source of autoantigens and endogenous adjuvants in the pathogenic model of systemic autoimmune diseases. This focus is justified in part because initial evidence in systemic lupus erythematosus (SLE) guided investigators toward the study of apoptosis, but also because other forms of cell death were unknown. To date, it is known that many other forms of cell death occur, and that they vary in their capacity to stimulate as well as inhibit the immune system. Among these, NETosis (an antimicrobial form of death in neutrophils in which nuclear material is extruded from the cell forming extracellular traps), is gaining major interest as a process that may trigger some of the immune features found in SLE, granulomatosis with polyangiitis (formerly Wegener’s granulomatosis) and Felty’s syndrome. Although there have been volumes of very compelling studies published on the role of cell death in autoimmunity, no unifying theory has been adopted nor have any successful therapeutics been developed based on this important pathway. The recent inclusion of NETosis into the pathogenic model of autoimmune diseases certainly adds novel insights into this paradigm, but also reveals a previously unappreciated level of complexity and raises many new questions. This review discusses the role of cell death in systemic autoimmune diseases with a focus on apoptosis and NETosis, highlights the current short comings in our understanding of the vast complexity of cell death, and considers the potential shift in the cell death paradigm in autoimmunity. Understanding this complexity is critical in order to develop tools to clearly define the death pathways that are active in systemic autoimmune diseases, identify drivers of disease propagation, and develop novel therapeutics.

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“…And, given the common availability of commercial assays, anti-MPO and anti-PR3 titers have been frequently assessed in SLE patients (Nassberger et al, 1990; Cambridge et al, 1994; Manolova et al, 2001; Pan et al, 2008). The available data is heterogeneous and no clear trend has emerged, although one can be relatively confident in saying that—at least for the assays that are commercially available—anti-MPO/PR3 autoantibodies do not specifically identify SLE patients, nor do they track with specific disease manifestations.…”

Section: Net Proteins and Slementioning

confidence: 99%

“…Both the iron-chelator lactoferrin and the serine protease cathepsin G have been objectively identified in PMA-induced NETs (Urban et al, 2009), and both appear to function as autoantigens in SLE (Lee et al, 1992; Galeazzi et al, 1998; Zhao et al, 1998; Manolova et al, 2001; Caccavo et al, 2005); although, again, no clear clinical correlation has emerged. In terms of circulating protein, there is no correlation between plasma lactoferrin and either active or inactive SLE (Adeyemi et al, 1990; Tsai et al, 1991), while cathepsin G protein levels have not been considered.…”

Section: Net Proteins and Slementioning

confidence: 99%

Proteins derived from neutrophil extracellular traps may serve as self-antigens and mediate organ damage in autoimmune diseases

Knight¹,

Carmona‐Rivera²,

Kaplan³

2012

Front. Immun.

154

112

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Neutrophils are the most abundant leukocytes in circulation and represent one of the first lines of defense against invading pathogens. Neutrophils possess a vast arsenal of antimicrobial proteins, which can be released from the cell by a death program termed NETosis. Neutrophil extracellular traps (NETs) are web-like structures consisting of decondensed chromatin decorated with granular and cytosolic proteins. Both exuberant NETosis and impaired clearance of NETs have been implicated in the organ damage of autoimmune diseases, such as systemic lupus erythematosus (SLE), small vessel vasculitis (SVV), and psoriasis. NETs may also represent an important source of modified autoantigens in SLE and SVV. Here, we review the autoimmune diseases linked to NETosis, with a focus on how modified proteins externalized on NETs may trigger loss of immune tolerance and promote organ damage.

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Antineutrophil cytoplasmic antibodies in patients with systemic lupus erythematosus: prevalence, antigen specificity, and clinical associations

Cited by 54 publications

References 30 publications

Anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus

Anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus

NETs: the missing link between cell death and systemic autoimmune diseases?

Proteins derived from neutrophil extracellular traps may serve as self-antigens and mediate organ damage in autoimmune diseases

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