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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: Oct 21, 2025

Intraoperative Detection of Subtle Endometriosis: A Novel Paradigm for Detection and Treatment of Pelvic Pain Associated with the Loss of Peritoneal Integrity
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The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis.

Chiara Agostinis1, Sonia Zorzet2, Andrea Balduit2

  • 1Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy.

Frontiers in Immunology
|September 7, 2021
PubMed
Summary

The complement system protein C3 is locally produced in endometriosis, promoting cyst formation and mast cell activation. C3 deficiency reduces endometriosis severity in mice, suggesting C3 as a potential therapeutic target.

Keywords:
C3TNF-αcomplement systemendometriosismast cells

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Area of Science:

  • Immunology
  • Oncology
  • Reproductive Medicine

Background:

  • The complement system is crucial for innate immunity, but also implicated in inflammation and cancer.
  • Endometriosis (EM) shares cancer-like invasive properties and involves immune evasion.
  • Ectopic endometrial cells in EM may produce complement component C3.

Purpose of the Study:

  • To investigate the role of locally synthesized C3 in endometriosis.
  • To explore C3's contribution to EM pathogenesis and cyst development.
  • To evaluate C3 as a potential biomarker and therapeutic target for EM.

Main Methods:

  • Immunofluorescence and RT-qPCR to detect C3 in ectopic vs. eutopic endometrial tissue.
  • Murine model of EM created by peritoneal injection of minced uterine tissue.
  • Analysis of cyst formation, mast cell degranulation, and C3a levels in wild-type vs. C3 knockout mice.

Main Results:

  • Locally synthesized C3 was detected in ectopic endometriotic tissue but not eutopic tissue.
  • C3 knockout mice exhibited reduced peritoneal cyst formation compared to wild-type mice.
  • Wild-type mice with EM showed increased mast cell degranulation and higher C3a levels, indicating an auto-amplifying pathogenic loop.

Conclusions:

  • Local C3 synthesis contributes to endometriosis progression by promoting cyst engraftment and mast cell activation.
  • C3 plays a pathogenic role in EM, potentially through C3a-mediated inflammation.
  • C3 is a potential biomarker for EM and a target for novel therapeutic strategies.