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Related Experiment Video

Updated: Mar 18, 2026

Depletion of Specific Cell Populations by Complement Depletion

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Self-nonself discrimination by the complement system.

Seppo Meri^1,2,3

¹Immunobiology, Research Programs Unit, Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Finland.

|July 10, 2016

Summary

This summary is machine-generated.

The alternative pathway (AP) of complement uses factor H to distinguish self from nonself, protecting host cells. Factor H mutations cause disease, and pathogens exploit it for survival.

Keywords:

escape hemolytic uremic syndrome sialic acid

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Last Updated: Mar 18, 2026

Depletion of Specific Cell Populations by Complement Depletion

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Published on: October 8, 2012

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

Area of Science:

Immunology
Molecular Biology

Background:

The alternative pathway (AP) of complement is crucial for innate immunity.
It distinguishes self from nonself using C3b and factor H.
Factor H binds polyanions on self-cells, preventing complement attack.

Purpose of the Study:

To elucidate the role of factor H in self-nonself discrimination by the AP.
To understand how factor H mutations lead to disease.
To investigate pathogen evasion strategies involving factor H.

Main Methods:

Biochemical assays to study factor H binding.
Genetic analysis of factor H mutations.
Microbial binding assays.

Main Results:

Factor H's polyanion-binding sites are key for recognizing self.
Factor H mutations are linked to hemolytic uremic syndrome and damage to blood and endothelial cells.
Pathogenic microbes bind factor H, evading complement-mediated destruction.

Conclusions:

Factor H is essential for preventing autoimmune complement attack.
Defects in factor H cause severe diseases, including kidney and brain damage.
Pathogen binding of factor H is a mechanism for immune evasion.