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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Related Experiment Video

Updated: Apr 12, 2026

Morphological and Compositional Analysis of Neutrophil Extracellular Traps Induced by Microbial and Chemical Stimuli
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Neutrophil extracellular traps can activate alternative complement pathways.

H Wang1,2,3,4,5, C Wang1,2,3,4,5, M-H Zhao1,2,3,4,5

  • 1Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China.

Clinical and Experimental Immunology
|May 13, 2015
PubMed
Summary
This summary is machine-generated.

Neutrophil extracellular traps (NETs) activate the alternative complement pathway. This finding suggests NETs contribute to anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) pathogenesis.

Keywords:
ANCAalternative complement pathwaycomplementneutrophil extracellular trapsvasculitis

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Area of Science:

  • Immunology
  • Pathogenesis of Vasculitis

Background:

  • Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) involves neutrophil interactions and complement activation.
  • Neutrophil extracellular traps (NETs) are increasingly recognized in AAV development, but their link to the alternative complement pathway is unclear.

Purpose of the Study:

  • To investigate the relationship between NETs and the alternative complement pathway in the context of AAV.

Main Methods:

  • In vitro detection of complement components on NETs using immunostaining and confocal microscopy.
  • Measurement of complement levels in serum supernatants incubated with NETs via ELISA.
  • Assessment of complement deposition after incubation with various treated human sera.

Main Results:

  • Complement factors B (Bb) and properdin were detected on NETs.
  • NETs induced by ANCA could activate the alternative complement cascade.
  • Degradation of NETs significantly reduced complement activation products (C3a, C5a, SC5b-9).

Conclusions:

  • Neutrophil extracellular traps (NETs) activate the alternative complement pathway.
  • NETs may play a role in the pathogenesis of anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV).