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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

Rheumatoid factor, complement, and mixed cryoglobulinemia.

Peter D Gorevic¹

¹Mount Sinai School of Medicine, Division of Rheumatalogy, Annenberg Building, Room 21-056, One Gustave L. Levy Place, New York, NY, USA. peter.gorevic@mountsinai.org

Clinical & Developmental Immunology

|September 8, 2012

Summary

Low serum complement component 4 (C4) in mixed cryoglobulinemia (MC) is linked to complement activation. This may involve classical, alternative, or lectin pathways, especially with hepatitis C virus (HCV) infection.

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Area of Science:

Immunology
Complement System Biology

Background:

Mixed cryoglobulinemia (MC) is associated with low serum levels of complement component 4 (C4).
Complement activation, particularly via the classical pathway, is implicated in the pathogenesis of MC.
Hepatitis C virus (HCV) infection can contribute to immune stimulation and complement pathway activation in MC.

Purpose of the Study:

To investigate the mechanisms of complement activation in mixed cryoglobulinemia.
To explore the role of various complement pathways (classical, alternative, lectin) in MC.
To understand the contribution of hepatitis C virus (HCV) to complement dysregulation in MC.

Main Methods:

Analysis of complement component 4 (C4) serum levels.
Investigation of complement activation pathways, including classical, alternative, and lectin pathways.
Assessment of immune complex (IC) formation, clearance, and localization.

Main Results:

Low C4 levels in MC suggest in vivo or ex vivo complement activation.
Potential activators include monoclonal IgM rheumatoid factor (RF), IgG antibodies, and cryocomplexes.
HCV infection may drive alternative and lectin pathway activation.
Immune complexes (ICs) localize to microcirculations, with defective clearance contributing to persistence.
Complement activation generates phlogistic fragments and the membrane attack complex (C5b-9).

Conclusions:

Complement activation is a key feature of mixed cryoglobulinemia (MC), contributing to its pathology.
Understanding complement activation pathways in MC, especially in HCV infection, is crucial.
Further research should focus on the effector mechanisms and viral contributions to complement activation in MC.