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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

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Enrichment of Bruch's Membrane from Human Donor Eyes

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Systemic complement activation in age-related macular degeneration.

Hendrik P N Scholl¹, Peter Charbel Issa, Maja Walier

¹Department of Ophthalmology, University of Bonn, Bonn, Germany.

|July 4, 2008

Summary

Systemic complement activation, particularly of the alternative pathway, is elevated in age-related macular degeneration (AMD) patients. This suggests AMD is a systemic disease linked to genetic factors like CFH.

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Area of Science:

Ophthalmology
Immunology
Genetics

Background:

Age-related macular degeneration (AMD) is a leading cause of blindness in the elderly.
Dysregulation of the alternative pathway (AP) of the complement cascade is implicated in AMD pathogenesis.
The hypothesis tested is that defective complement activation control underlies AMD.

Purpose of the Study:

To determine parameters of complement activation in blood plasma of AMD patients and controls.
To correlate complement activation markers with disease-associated genetic markers in AMD.
To investigate the systemic nature of complement activation in AMD.

Main Methods:

Quantified plasma concentrations of complement activation products (C3d, Ba, C3a, C5a, SC5b-9) and proteins (C3, C4, factor B, factor H, factor D) in 112 AMD patients and 67 controls.
Analyzed single nucleotide polymorphisms (SNPs) in complement genes: factor H (CFH), factor B-C2 (BF-C2), and complement C3 (C3).
Used logistic regression to compare the discriminative accuracy of complement activation markers versus genetic markers.

Main Results:

Significantly elevated levels of all complement activation products, especially Ba and C3d, were observed in AMD patients (p<0.001).
Factor D levels were also altered in AMD patients, unlike C3, C4, or factor H.
A model using complement activation markers (Ba, C3d, factor D) showed better discriminative accuracy for AMD than a model based on genetic markers.

Conclusions:

This study provides the first evidence of systemic complement activation in AMD patients, suggesting AMD is a systemic disease.
Systemic activation of the alternative complement pathway is associated with genetic variants of CFH previously linked to AMD susceptibility.
The findings highlight the role of complement dysregulation in AMD pathogenesis and suggest potential therapeutic targets.