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Related Concept Videos

Complement System01:27

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...
Antibody Actions01:26

Antibody Actions

Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
Neutralization
Antibodies can bind to pathogens, preventing them from infecting host cells. This process...
Antimicrobial Proteins01:23

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 Tests00:49

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...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

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...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...

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A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.

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Related Experiment Video

Updated: Jun 10, 2026

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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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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The role of complement in AMD.

Peter F Zipfel1, Nadine Lauer, Christine Skerka

  • 1Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Beutenbergstrasse 11a, Jena, Germany. peter.zipfel@hki-jena.de

Advances in Experimental Medicine and Biology
|August 17, 2010
PubMed
Summary
This summary is machine-generated.

Genetic variations in complement genes like Factor H increase age-related macular degeneration (AMD) risk. However, deletions in the Factor H gene cluster offer protection against AMD development.

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Area of Science:

  • Ophthalmology
  • Immunology
  • Genetics

Background:

  • Age-related macular degeneration (AMD) is a leading cause of vision loss.
  • Genetic variations in complement genes are associated with AMD risk.
  • The alternative complement pathway plays a role in AMD pathogenesis.

Purpose of the Study:

  • To describe the role of complement in the retina.
  • To summarize current concepts of complement dysregulation in AMD.
  • To investigate genetic factors influencing AMD risk and protection.

Main Methods:

  • Analysis of genetic variations in complement genes.
  • Review of the role of complement pathway in retinal inflammation.
  • Examination of Factor H and FHL1 sequence variations.

Main Results:

  • Specific variations in complement genes (Factor H, C3, Factor B, C2, Factor I) confer AMD risk.
  • Deletion of CFHR1 and CFHR3 provides a protective effect against AMD.
  • A sequence variation at position 402 in Factor H/FHL1 (tyrosine protective, histidine risk) is strongly associated with AMD.

Conclusions:

  • Defective or inappropriate local complement control contributes to AMD pathophysiology.
  • Complement dysregulation leads to retinal inflammation, drusen formation, and vision loss.
  • Understanding complement's role offers potential therapeutic targets for AMD.