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Human erythrocytes inhibit complement-mediated solubilization of immune complexes.
B L Dorval1, F G Cosio, D J Birmingham
1Department of Internal Medicine, Ohio State University College of Medicine, Columbus 43210-1228.
Journal of Immunology (Baltimore, Md. : 1950)
|April 15, 1989
Summary
Human red blood cells (E) inhibit the solubilization and complement activation of immune complexes (IC). This occurs because E bind to IC, preventing complement system engagement and promoting IC clearance.
Area of Science:
- Immunology
- Complement System Biology
- Cellular Immunology
Background:
- Precipitable immune complexes (IC) are typically solubilized by the complement system.
- Red blood cells (E) can interact with complement components and immune complexes.
- The role of E in modulating IC-mediated complement activation and solubilization is not fully understood.
Purpose of the Study:
- To investigate the inhibitory effect of human E on IC solubilization.
- To determine the mechanism by which E influence complement activation by IC.
- To evaluate the role of complement receptor type 1 (CR1) in E-mediated inhibition.
Main Methods:
- Incubation of precipitable IC with human or guinea pig serum.
- Addition of human E or SRBC to IC-serum mixtures.
- Treatment of human E with trypsin or anti-CR1 monoclonal antibodies (mAb).
- Measurement of complement component activation (C3, C5, C4) and C3b deposition.
Main Results:
- Human E significantly inhibited IC solubilization by binding to IC.
- SRBC did not bind IC or inhibit solubilization.
- E-mediated inhibition of solubilization was independent of CR1.
- Human E significantly inhibited complement activation (C3 and C5) by IC.
- C3b generated during IC activation deposited on both IC and E, suggesting competition for C3.
Conclusions:
- Human E inhibit complement-mediated solubilization of IC.
- Human E actively inhibit complement activation triggered by IC.
- E may compete for nascent C3, thereby modulating complement activation and IC processing.