Dr. Kämpe has applications for patents on two novel autoantigens.
Systemic Sclerosis Basic Science Studies
Lack of evidence of stimulatory autoantibodies to platelet-derived growth factor receptor in patients with systemic sclerosis
Article first published online: 30 MAR 2009
Copyright © 2009 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 60, Issue 4, pages 1137–1144, April 2009
How to Cite
Classen, J.-F., Henrohn, D., Rorsman, F., Lennartsson, J., Lauwerys, B. R., Wikström, G., Rorsman, C., Lenglez, S., Franck-Larsson, K., Tomasi, J.-P., Kämpe, O., Vanthuyne, M., Houssiau, F. A. and Demoulin, J.-B. (2009), Lack of evidence of stimulatory autoantibodies to platelet-derived growth factor receptor in patients with systemic sclerosis. Arthritis & Rheumatism, 60: 1137–1144. doi: 10.1002/art.24381
- Issue published online: 30 MAR 2009
- Article first published online: 30 MAR 2009
- Manuscript Accepted: 8 DEC 2008
- Manuscript Received: 22 FEB 2008
- Foundation for Scientific Research, Belgium
Systemic sclerosis (SSc) is a severe connective tissue disease of unknown etiology, characterized by fibrosis of the skin and multiple internal organs. Recent findings suggested that the disease is driven by stimulatory autoantibodies to platelet-derived growth factor receptor (PDGFR), which stimulate the production of reactive oxygen species (ROS) and collagen by fibroblasts. These results opened novel avenues of research into the diagnosis and treatment of SSc. The present study was undertaken to confirm the presence of anti-PDGFR antibodies in patients with SSc.
Immunoglobulins from 37 patients with SSc were purified by protein A/G chromatography. PDGFR activation was tested using 4 different sensitive bioassays, i.e., cell proliferation, ROS production, signal transduction, and receptor phosphorylation; the latter was also tested in a separate population of 7 patients with SSc from a different research center.
Purified IgG samples from patients with SSc were positive when tested for antinuclear autoantibodies, but did not specifically activate PDGFRα or PDGFRβ in any of the tests. Cell stimulation with PDGF itself consistently produced a strong signal.
The present results raise questions regarding the existence of agonistic autoantibodies to PDGFR in SSc.