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Control of immune complexes by the classical pathway.
Behring Institute Mitteilungen
|July 1, 1989
Summary
The complement system prevents immune complex disease (ICD) by keeping antibody-antigen complexes soluble. A glycoprotein (gp60) in serum inhibits this process, particularly in rheumatoid arthritis (RA) patients.
Area of Science:
- Immunology
- Biochemistry
Background:
- Inherited deficiencies in classical complement components (C1q-C3) are linked to immune complex disease (ICD).
- The complement system protects against ICD by maintaining small, soluble antigen-antibody complexes (IC).
Purpose of the Study:
- To investigate the mechanisms by which complement prevents immune precipitation (PIP) and solubilizes immune precipitates (SOL).
- To identify factors in patient sera that inhibit PIP, contributing to ICD development.
Main Methods:
- Examined the roles of classical and alternative complement pathways in PIP and SOL.
- Investigated inhibitors of PIP in patient sera, including a purified glycoprotein (gp60).
Main Results:
- The classical pathway is crucial for PIP, while the alternative pathway supports SOL, with optimal SOL requiring an intact classical pathway.
- A novel inhibitor, gp60, was purified; it binds IgG Fc, competes with C1q, and inhibits C1 activation, thus preventing PIP.
- Gp60 is present in normal serum and elevated in rheumatoid arthritis (RA) sera, suggesting its role in ICD pathogenesis.
Conclusions:
- The classical complement pathway is vital for preventing immune complex precipitation and disease.
- A serum glycoprotein (gp60) inhibits complement-mediated protection against ICD by interfering with C1 activation.
- Understanding gp60's role may offer new therapeutic targets for immune complex diseases like RA.