Evidence map›Paper›PMID 26658004›Full record

ReviewJournal of leukocyte biology2016

At the Bedside: Neutrophil extracellular traps (NETs) as targets for biomarkers and therapies in autoimmune diseases.

April Barnado, Leslie J Crofford, Jim C Oates

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

94 citing papers in PubMed, 169 citations in OpenAlex.

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34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

April Barnado*Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA; and Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA april.barnado@vanderbilt.edu.
Leslie J Crofford*Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA; and Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Jim C Oates*Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA; and Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Vanderbilt University · USMedical University of South Carolina · US

Funding

Interdisciplinary Training in Rheumatic DiseasesT32AR059039 · NIAMS · VANDERBILT UNIVERSITY · PI Tracy Minan Frech, AMY S MAJOR · 2010 to 2026
$4.3M
NIAMS NIH HHS T32 AR059039
6 · The paper itself

Abstract

Neutrophil extracellular traps are associated with a unique form of cell death distinct from apoptosis or necrosis, whereby invading microbes are trapped and killed. Neutrophil extracellular traps can contribute to autoimmunity by exposing autoantigens, inducing IFN-α production, and activating the complement system. The association of neutrophil extracellular traps with autoimmune diseases, particularly systemic lupus erythematosus, will be reviewed. Increased neutrophil extracellular trap formation is seen in psoriasis, antineutrophil cytoplasmic antibody-associated vasculitis, antiphospholipid antibody syndrome rheumatoid arthritis, and systemic lupus erythematosus. Neutrophil extracellular traps may promote thrombus formation in antineutrophil cytoplasmic antibody-associated vasculitis and antiphospholipid antibody syndrome. In systemic lupus erythematosus, increased neutrophil extracellular trap formation is associated with increased disease activity and renal disease, suggesting that neutrophil extracellular traps could be a disease activity marker. Neutrophil extracellular traps can damage and kill endothelial cells and promote inflammation in atherosclerotic plaques, which may contribute to accelerated atherosclerosis in systemic lupus erythematosus. As neutrophil extracellular traps induce IFN-α production, measuring neutrophil extracellular traps may estimate IFN-α levels and identify which systemic lupus erythematosus patients have elevated levels and may be more likely to respond to emerging anti-IFN-α therapies. In addition to anti-IFN-α therapies, other novel agents, such as N-acetyl-cysteine, DNase I, and peptidylarginine deiminase inhibitor 4, target neutrophil extracellular traps. Neutrophil extracellular traps offer insight into the pathogenesis of autoimmune diseases and provide promise in developing disease markers and novel therapeutic agents in systemic lupus erythematosus. Priority areas for basic research based on clinical research insights will be identified, specifically the potential role of neutrophil extracellular traps as a biomarker and therapeutic target in systemic lupus erythematosus.

Indexed as

Molecular Targeted TherapyAcetylcysteineAntibodies, MonoclonalAntimalarialsAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisApoptosisAtherosclerosisAutoantigensAutoimmune DiseasesBiomarkersDeoxyribonuclease IExtracellular TrapsFemaleHumansHydrolasesImmunosuppressive AgentsAcetylcysteineAntibodies, MonoclonalAntimalarialsAutoantigensBiomarkersDeoxyribonuclease IHydrolasesImmunosuppressive AgentsInterferon-alphaPADI4 protein, humanProtein-Arginine DeiminasesProtein-Arginine Deiminase Type 4Vitamin Dautoimmunitysystemic lupus erythematosustype I IFN

Identifiers

PMID26658004
PMCPMC6608010
OpenAlexW2203663529

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.