Centres Austria   
  Prof. Josef Smolen
Personal Professor Josef Smolen is based in the Department of Rheumatology, Internal Medicine III, at the Medical University of Vienna, in Austria. The department is currently training 3 fellows per year, and also hosts PhD students.
Interests Professor Smolen’s department is a rheumatology referral center, with clinical practice focussing on rheumatoid arthritis (RA), early arthritis, spondylarthropathies, connective tissue diseases, hand osteoarthritis, and osteoporosis.
Research activities include clinical trials and outcomes research, in addition to laboratory-based research in the fields of experimental arthritis, autoimmunity, in vivo imaging, proinflammatory cytokines, and cellular immunology.
Research
Projects 		1. Concepts important for people with rheumatic diseases
2. Outcomes assessment in RA
3. Pathogenetic pathways in experimental arthritis
Recent
Publications

Stamm TA, Bauernfeind B, Coenen M, Feierl E, Mathis M, Stucki G, Smolen JS, Machold KP, Aringer M.
Concepts important to persons with systemic lupus erythematosus and their coverage by standard measures of disease activity and health status. Arthritis Rheum. 2007;57:1287-1295.

Aletaha D, Funovits J, Keystone EC, Smolen JS.
Disease activity early in the course of treatment predicts response to therapy after one year in rheumatoid arthritis patients. Arthritis Rheum. 2007;56:3226-3235.

Bonelli M, von Dalwigk K, Savitskaya A, Smolen JS, Scheinecker C.
Foxp3 expression in CD4+ T cells of patients with systemic lupus erythematosus (SLE): A comparative phenotypic analysis. Ann Rheum Dis. 2007;epub ahead of print

Zwerina J, Redlich K, Polzer K, Joosten L, Krönke G, Distler J, Hess A, Pundt N, Pap T, Hoffmann O, Gasser J, Scheinecker C, Smolen JS, van den Berg W, Schett G.
TNF-induced structural joint damage is mediated by IL-1. Proc Natl Acad Sci USA. 2007;104:11742-7. Epub ahead of print.

Bobacz K, Sunk IG, Hofstaetter JG, Amoyo L, Toma CD, Akira S, Weichhart T, Saemann M, Smolen JS.
Toll-like receptors and chondrocytes: the lipopolysaccharide-induced decrease in cartilage matrix synthesis is dependent on the presence of toll-like receptor 4 and antagonized by bone morphogenetic protein 7. Arthritis Rheum. 2007;56:1880-1893.
   
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