Sera from anti–Jo-1–positive patients with polymyositis and interstitial lung disease induce expression of intercellular adhesion molecule 1 in human lung endothelial cells
Version of Record online: 30 JUL 2009
Copyright © 2009 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 60, Issue 8, pages 2524–2530, August 2009
How to Cite
Helmers, S. B., Englund, P., Engström, M., Åhlin, E., Fathi, M., Janciauskiene, S., Heimbürger, M., Rönnelid, J. and Lundberg, I. E. (2009), Sera from anti–Jo-1–positive patients with polymyositis and interstitial lung disease induce expression of intercellular adhesion molecule 1 in human lung endothelial cells. Arthritis & Rheumatism, 60: 2524–2530. doi: 10.1002/art.24683
- Issue online: 30 JUL 2009
- Version of Record online: 30 JUL 2009
- Manuscript Accepted: 15 APR 2009
- Manuscript Received: 19 SEP 2007
- European Union Sixth Framework Programme. Grant Number: project AutoCure; LSH-018661
- Swedish Research Council. Grant Number: 2002-74X-14045-02A
- Vårdal Foundation
- Swedish Rheumatism Association
- King Gustaf V's 80-Year Foundation
- Börje Dahlin's Foundation
- Professor Nanna Svartz' Foundation
- Magnus Bergvall Foundation
- Stiftelsen Clas Groschinskys Minnesfond
- Karolinska Institutet Foundation
To investigate whether sera or purified IgG from patients with polymyositis (PM) and patients with dermatomyositis (DM), with or without interstitial lung disease (ILD), can activate endothelial cells (ECs).
Patients' sera were selected based on the presence or absence of anti–Jo-1, anti-SSA, or anti–U1 small nuclear RNP autoantibodies. The presence of autoantibodies was determined by line blot assays. Cultured human microvascular ECs derived from lung tissue (HMVEC-L) were incubated with sera or purified IgG from 22 patients with PM, 7 patients with DM, and 10 healthy individuals as controls. Assessment of intercellular adhesion molecule 1 (ICAM-1) expression was conducted by immunofluorescence (n = 22) and by cell-based enzyme-linked immunosorbent assay (ELISA) (n = 20). Serum levels of soluble ICAM-1 (sICAM-1) were determined by ELISA.
Sera from PM patients with ILD who were positive for anti–Jo-1 autoantibodies had a significantly stronger effect on the expression of ICAM-1 by HMVEC-L in comparison with sera from healthy controls and patients with other autoantibodies. Purified IgG did not induce ICAM-1 expression. Higher serum levels of sICAM-1 were found in patients with myositis compared with healthy controls.
EC activation with ICAM-1 expression could contribute to the multiorgan involvement, including the development of myositis and ILD, in patients carrying anti–Jo-1 autoantibodies. The EC-activating factors are not the autoantibodies themselves, but might be systemic factors associated with these autoantibodies.