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Updated: Jun 18, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
Published on: January 29, 2014
Immune complex modulation by plasma proteins. With special reference to the complement system and autoimmune
1Institute of Medical Microbiology, University of Odense.
The complement system
Area of Science:
- Immunology
- Biochemistry
Background:
- The complement (C) system, comprising classical and alternative pathways, interacts with immune complexes (IC).
- C activation by IC influences IC properties, affecting solubility, phagocytosis, and inflammation.
- Dysregulated IC-C interaction can lead to chronic inflammatory diseases.
Purpose of the Study:
- To review aspects of IC-C interactions.
- To develop and characterize an assay for measuring C activity in solubilizing fluid-phase IC (CMS assay).
- To investigate the correlation between CMS capacity, disease activity, and C factors in patients with systemic inflammatory diseases.
Main Methods:
- Development of a complement-mediated solubilization (CMS) assay for fluid-phase IC.
- Characterization of the CMS assay by varying C deficiencies, divalent metal ions, temperature, and ionic strength.
- Analysis of serum from patients with systemic lupus erythematosus (SLE) and other inflammatory conditions using the CMS assay.
- Investigation of potential CMS inhibitors in SLE patient sera using HPLC.
Main Results:
- The CMS assay is dependent on the alternative C pathway and facilitated by the classical pathway.
- Serum from SLE and other inflammatory disease patients showed reduced IC solubilization capacity (CMS).
- Reduced CMS capacity correlated inversely with disease activity in SLE patients.
- A novel CMS inhibitor was identified in some SLE sera, potentially linked to incompletely solubilized IC.
Conclusions:
- The CMS assay effectively measures C activity in IC solubilization.
- Reduced CMS capacity and presence of inhibitors may contribute to IC-mediated inflammatory diseases like SLE.
- Further research into CMS inhibitors and their role in SLE pathogenesis is warranted.
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