Drs. Chowdhry and Kowal contributed equally to this work.
Autoantibodies that bind glomeruli: Cross-reactivity with bacterial antigen
Article first published online: 28 JUL 2005
Copyright © 2005 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 52, Issue 8, pages 2403–2410, August 2005
How to Cite
Chowdhry, I. A., Kowal, C., Hardin, J., Zhou, Z. and Diamond, B. (2005), Autoantibodies that bind glomeruli: Cross-reactivity with bacterial antigen. Arthritis & Rheumatism, 52: 2403–2410. doi: 10.1002/art.21143
- Issue published online: 28 JUL 2005
- Article first published online: 28 JUL 2005
- Manuscript Accepted: 8 APR 2005
- Manuscript Received: 30 JUN 2004
- National Institute of Arthritis and Musculoskeletal and Skin Diseases
- New York Chapter of the Arthritis Foundation
Systemic lupus erythematosus (SLE) is characterized by the production of multiple autoantibodies. Anti-DNA antibodies are associated with glomerulonephritis in SLE. It has been shown that anti-DNA antibodies cross-react with bacterial polysaccharide and, thus, might be elicited by microbial exposure. Non–DNA-binding antibodies also contribute significantly to the pathogenesis of lupus nephritis. The goal of this study was to characterize non–DNA-binding, kidney-binding antibodies.
We generated a combinatorial library derived from spleen cells of a patient with SLE who had just previously received pneumococcal vaccine. The phage library was used in an in vivo biopanning technique to identify non–DNA-binding, kidney-binding antibodies. Antibodies were then analyzed for binding to bacterial polysaccharide and to renal antigens.
Eight antibodies were characterized that bound glomeruli, but not DNA. All antibodies isolated by this protocol were IgG class, suggesting that there is affinity maturation for glomerular binding. Four of the antibodies cross-reacted with pneumococcal polysaccharide. Six of the antibodies bound to renal antigens that have previously been reported to be cross-reactive with DNA; the other 2 bound to histone.
This study suggests that both DNA-binding and non–DNA-binding antibodies in SLE may be elicited by the same bacterial antigens.