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Complement System

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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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Coagulation

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Related Experiment Video

Updated: Mar 9, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

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Properdin binding to complement activating surfaces depends on initial C3b deposition.

Morten Harboe¹, Christina Johnson¹, Stig Nymo²

¹Department of Immunology, Oslo University Hospital, Rikshospitalet, 0424 Oslo, Norway.

Proceedings of the National Academy of Sciences of the United States of America

|January 11, 2017

Summary

This summary is machine-generated.

Properdin

Keywords:

C3 Neisseria meningitidis complement myeloperoxidase properdin

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Area of Science:

Immunology
Complement System Biology

Background:

Properdin's role as a pattern recognition molecule is debated.
Previous studies suggest properdin binding is secondary to C3 deposition.

Purpose of the Study:

To investigate the C3-dependence of properdin binding to various targets.
To challenge the established view of properdin as a pattern recognition molecule.

Main Methods:

Experiments using human serum, C3-depleted serum, and C3-inhibitors.
Flow cytometry to detect properdin binding to cells and bacteria.
Binding assays with myeloperoxidase and endothelial cells.

Main Results:

Properdin binding to myeloperoxidase, endothelial cells, and Neisseria meningitidis is C3-dependent.
Properdin binding requires prior C3 activation, not direct pattern recognition.

Conclusions:

Properdin's binding is contingent on C3 activation, questioning its role as a primary pattern recognition molecule.
Careful control of C3 activation is crucial for studying properdin's function.