Deficiency of complement component C3 is associated with accelerated removal of soluble 123I‐labelled aggregates of IgG from the circulation

• Published in: Clinical and experimental immunology 1992-12, Vol.90 (3), p.394-400
• Main Authors: HALMA, C., DAHA, M. R., CAMPS, J. A. J., EVERS‐SCHOUTEN, J. H., PAUWELS, E. K. J., ES, L. A.
• Format: Article
• Language: English
• Subjects: Adult; Antigen-Antibody Complex; Biological and medical sciences; Complement C3 - deficiency; complement deficiency C3; complement receptor type 1; CR1, CD35; Erythrocytes - metabolism; Erythrocytes - ultrastructure; Female; Humans; IgG aggregates; immune complexes; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunoglobulin G - blood; Immunoglobulin G - metabolism; Immunopathology; Iodine Radioisotopes; Male; Medical sciences; Oxygen - metabolism; Protein Binding; Receptors, Complement 3b - immunology; Receptors, Complement 3b - physiology
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1992.tb05857.x

SUMMARY Complement and erythrocyte complement receptors CR1 (CD35) play an important role in the clearance of immune complexes. We studied the elimination of soluble 123I‐labelled aggregates of human immunoglobulin G (123I‐AIgG), used as a model for immune complexes, in two patients with a congenital and two patients with an acquired deficiency of complement component C3, and compared these with 10 healthy controls. The first disappearance halflife of 123I‐AIgG was shorter (3.3 ± 04 versus 70 ± 0.4 min in the controls, P= 0.005) and maximal hepatic uptake of aggregates was increased in the C3 deficient patients (maximal liver/background ratio 3.6 ± 0.4 versus 2.7 ± 0.2 in controls, P= 0.04). Apparently, in the absence of C3, removal of circulating immune complexes by the liver is accelerated, probably through Fc receptor‐dependent mechanisms.