Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

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...

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...

Hypersensitivity Reactions: Immune-Complex Reactions

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

Antimicrobial Proteins

Antimicrobial Proteins

Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...

Complementation Tests

Complementation Tests

A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...

Multiple Allele Traits

Multiple Allele Traits

The Concept of Multiple Allelism

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Heterogeneous immune cell composition in patients with combined immunodeficiency.

Frontiers in immunology·2026

Same author

Targets for disease modification in schizophrenia: New findings add to evidence for the involvement of the immune complement system.

Proceedings of the National Academy of Sciences of the United States of America·2026

Same author

Dysregulation of complement at the synapse in P301S mice and human tauopathies.

Acta neuropathologica communications·2026

Same author

Hyperglycemia promotes maladaptive Dectin-1 signaling and impairs skin antifungal host defense.

bioRxiv : the preprint server for biology·2026

Same author

Primary Amoebic Meningoencephalitis caused by Complement C2 Deficiency.

medRxiv : the preprint server for health sciences·2026

Same author

Activation of the Lectin Pathway Drives Persistent Complement Dysregulation in Long COVID.

Immunology·2026

Search research articles

Related Experiment Video

Updated: Jun 2, 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

Published on: July 18, 2017

Common polymorphisms in C3, factor B, and factor H collaborate to determine systemic complement activity and disease

Meike Heurich¹, Ruben Martínez-Barricarte, Nigel J Francis

¹Department of Infection, Immunity and Biochemistry, School of Medicine, Cardiff University, Cardiff CF14 4XN, United Kingdom.

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

|May 11, 2011

Summary

Genetic variations in complement proteins C3, factor B, and factor H influence the alternative pathway (AP) of complement. Specific combinations of these polymorphisms, termed a functional complotype, determine an individual's susceptibility to AP-driven diseases like AMD.

More Related Videos

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

Published on: May 19, 2020

Enrichment of Bruch's Membrane from Human Donor Eyes

Enrichment of Bruch's Membrane from Human Donor Eyes

Published on: November 15, 2015

Related Experiment Videos

Last Updated: Jun 2, 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

Published on: July 18, 2017

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

Published on: May 19, 2020

Enrichment of Bruch's Membrane from Human Donor Eyes

Enrichment of Bruch's Membrane from Human Donor Eyes

Published on: November 15, 2015

Area of Science:

Immunology
Genetics
Molecular Biology

Background:

Common polymorphisms in complement alternative pathway (AP) proteins C3, factor B (fB), and factor H (fH) are linked to age-related macular degeneration (AMD) and other diseases.
Previous research demonstrated fB(R32Q) affects C3 convertase formation and fH(V62I) impacts factor I cofactor activity.

Purpose of the Study:

To elucidate the functional impact of the C3(R102G) polymorphism on alternative pathway (AP) activity.
To investigate how combinations of common AP protein polymorphisms influence overall AP function and disease susceptibility.

Main Methods:

Hemolysis assays were employed to assess AP activation efficiency with different C3 variants.
Binding kinetics of factor H (fH) to C3b fragments were analyzed.
Add-back assays were performed using combinations of disease-associated and protective variants of C3, fB, and fH.

Main Results:

The C3(102G) variant demonstrated more efficient AP activation compared to C3(102R).
Factor H bound more strongly to C3b(102R) than C3b(102G), and fH cofactor activity was reduced for C3b(102G), promoting AP amplification.
Combinations of risk variants (C3(102G), fB(32R), fH(62V)) resulted in significantly higher hemolytic activity than protective variants (C3(102R), fB(32Q), fH(62I)).

Conclusions:

The C3(R102G) polymorphism influences AP activity by affecting C3b binding and fH cofactor function.
The concept of a functional complotype, defined by the combination of individual polymorphisms, is introduced.
This functional complotype can predict an individual's susceptibility to complement alternative pathway-driven diseases.