Assessment of the potential pathogenicity of type ii collagen autoantibodies in patients with rheumatoid arthritis. Evidence of restricted IgG3 subclass expression and activation of complement C5 to C5a

IgG subclass analysis by enzyme‐linked im‐munosorbent assay of the autoantibody to native type II collagen, detected in 9 patients with classic or definite rheumatoid arthritis, demonstrated a predominance of IgG3 autoantibody. Gm allotyping revealed no obvious association with a particular phenotyp...

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Bibliographic Details
Published in:Arthritis and rheumatism 1986-11, Vol.29 (11), p.1316-1321
Main Authors: Watson, W. C., Cremer, M. A., Wooley, P. H., Townes, A. S.
Format: Article
Language:English
Subjects:
Animals
Arthritis, Rheumatoid - etiology
Arthritis, Rheumatoid - immunology
Autoantibodies - analysis
Biological and medical sciences
Collagen - immunology
Complement Activation
Complement C5 - analysis
Complement C5a
Cross Reactions
Diseases of the osteoarticular system
Enzyme-Linked Immunosorbent Assay
Humans
Immunoglobulin G - analysis
Immunoglobulin Gm Allotypes - analysis
Inflammatory joint diseases
Medical sciences
Mice
Phenotype
Polysaccharides, Bacterial - immunology
Streptococcus pneumoniae - immunology
Tetanus Toxoid - immunology
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Summary:IgG subclass analysis by enzyme‐linked im‐munosorbent assay of the autoantibody to native type II collagen, detected in 9 patients with classic or definite rheumatoid arthritis, demonstrated a predominance of IgG3 autoantibody. Gm allotyping revealed no obvious association with a particular phenotype. In comparative studies, IgG antibodies to the capsular polysaccharides of pneumococci and tetanus toxoid protein in these same patients consisted predominantly of IgG2 and IgG4. Purified type II collagen autoantibody from 3 of these patients activated complement C5 to C5a when bound to human cartilage in vitro, as measured by radioim‐munoassay. These results represent direct evidence of a potential pathogenic role for this autoantibody in rheumatoid arthritis.
ISSN:0004-3591
1529-0131
DOI:10.1002/art.1780291103