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Complement System

Complement System

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 membrane...

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Related Experiment Video

Updated: Jun 6, 2026

Murine Model of Intestinal Ischemia-reperfusion Injury

Murine Model of Intestinal Ischemia-reperfusion Injury

Published on: May 11, 2016

Specific collaboration between rat membrane complement regulators Crry and CD59 protects peritoneum from damage by

Tomohiro Mizuno¹, Masashi Mizuno, B Paul Morgan

¹Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association

|November 25, 2010

Summary

Complement regulators Crry and CD59 control peritoneal inflammation during dialysis. Blocking these regulators causes injury, highlighting their importance in preventing peritoneal inflammation in patients undergoing peritoneal dialysis.

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Last Updated: Jun 6, 2026

Murine Model of Intestinal Ischemia-reperfusion Injury

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Published on: May 11, 2016

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

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Published on: May 19, 2020

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Published on: July 18, 2017

Area of Science:

Immunology
Renal Physiology
Cell Biology

Background:

The peritoneal cavity is a sterile environment crucial for peritoneal dialysis (PD).
Unregulated complement activation can cause peritoneal inflammation in PD patients.
Membrane complement regulators (CRegs) like Crry, CD55, and CD59 are present in the rat peritoneum.

Purpose of the Study:

To investigate the functional roles of CRegs in the peritoneal cavity.
To understand how CRegs control complement activation in the context of PD.

Main Methods:

Utilized blocking monoclonal antibodies against individual CRegs (Crry, CD55, CD59).
Assessed complement activation and peritoneal injury in rats with varying peritoneal dialysis fluid (PDF) compositions.
Confirmed findings using in vitro experiments with primary rat mesothelial cells.

Main Results:

Blocking a single CReg did not induce peritoneal injury.
Combined blockade of Crry and CD59 led to significant peritoneal tissue injury, inflammation, and edema.
Complement components C3 and C5b-9 deposition occurred after combined Crry and CD59 blockade.
Peritoneal injury was exacerbated by lower PDF pH and higher glucose concentrations.
In vitro studies corroborated the in vivo findings.

Conclusions:

Rat CRegs, specifically Crry and CD59, work together to regulate complement activation in the peritoneum.
Impairment of these CRegs during PD may lead to severe peritoneal inflammation.