Evidence map›Paper›PMID 25963026›Full record

ArticleClinical and experimental immunology2015

Neutrophil extracellular traps can activate alternative complement pathways.

H Wang, C Wang, M-H Zhao, M Chen

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 2 pooled it
13.9field-weighted citation impact, top 1% 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

121 citing papers in PubMed, 2 syntheses or guidelines pooled it, 179 citations in OpenAlex.

  1. Pooled it
  2. Neutrophil Extracellular Traps (NETs) and Vasculitis.International journal of medical sciences · 2021
    Pooled it
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  16. Role of platelets and NETs in arterial thrombosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  17. Disseminated intravascular coagulation.Journal of intensive care · 2025
    Review
  18. A Web of Challenges: The Therapeutic Struggle to Target NETs in Disease.International journal of molecular sciences · 2025
    Review
  19. Review
  20. Review

61 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

4 authors at 3 institutions in 1 country.

H WangRenal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
C WangRenal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
M-H ZhaoRenal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
M ChenRenal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
Peking University First Hospital · CNCenter for Life Sciences · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction between neutrophils and activation of alternative complement pathway plays a pivotal role in the pathogenesis of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). ANCAs activate primed neutrophils to release neutrophil extracellular traps (NETs), which have recently gathered increasing attention in the development of AAV. The relationship between NETs and alternative complement pathway has not been elucidated. The current study aimed to investigate the relationship between NETs and alternative complement pathway. Detection of components of alternative complement pathway on NETs in vitro was assessed by immunostain and confocal microscopy. Complement deposition on NETs were detected after incubation with magnesium salt ethyleneglycol tetraacetic acid (Mg-EGTA)-treated human serum. After incubation of serum with supernatants enriched in ANCA-induced NETs, levels of complement components in supernatants were measured by enzyme-linked immunosorbent assay (ELISA). Complement factor B (Bb) and properdin deposited on NETs in vitro. The deposition of C3b and C5b-9 on NETs incubated with heat-inactivated normal human serum (Hi-NHS) or EGTA-treated Hi-NHS (Mg-EGTA-Hi-NHS) were significantly less than that on NETs incubated with NHS or EGTA-treated NHS (Mg-EGTA-NHS). NETs induced by ANCA could activate the alternative complement cascade in the serum. In the presence of EGTA, C3a, C5a and SC5b-9 concentration decreased from 800·42 ± 244·81 ng/ml, 7·68 ± 1·50 ng/ml, 382·15 ± 159·75 ng/ml in the supernatants enriched in ANCA induced NETs to 479·07 ± 156·2 ng/ml, 4·86 ± 1·26 ng/ml, 212·65 ± 44·40 ng/ml in the supernatants of DNase I-degraded NETs (P < 0·001, P = 0·008, P < 0·001, respectively). NETs could activate the alternative complement pathway, and might thus participate in the pathogenesis of AAV.

Indexed as

Antibodies, Antineutrophil CytoplasmicAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisCells, CulturedComplement ActivationComplement C3aComplement C3bComplement C5aComplement Factor BComplement Membrane Attack ComplexComplement Pathway, AlternativeEgtazic AcidExtracellular TrapsHot TemperatureHumansImmunoblottingMicroscopy, ConfocalAntibodies, Antineutrophil CytoplasmicComplement C3aComplement C3bComplement C5aComplement Factor BComplement Membrane Attack ComplexEgtazic AcidProperdinSC5b-9 protein complexalternative complement pathwayANCAcomplementneutrophil extracellular trapsvasculitis

Identifiers

PMID25963026
PMCPMC4557387
OpenAlexW2109293981

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.