We conduct active translational and clinical research into rheumatic inflammatory diseases, especially rheumatoid arthritis, myositis, SLE, and Sjögren’s disease.
We do basic research into the origin of inflammatory disease in animal models, and conduct genetic and cell biology projects where we identify new molecular pathways to disease. We have recently identified several new molecular pathways that will contribute to the identification of new drug candidates.
Our epidemiological research aims to understand which environmental factors interact with genes that confer susceptibility to disease that gives rise to RA and myositis. We have identified several such factors and have found a significantly elevated risk of developing disease; for example, in individuals with certain risk genes who are exposed to tobacco smoke or rock dust. This research facilitates improved primary prevention of rheumatic inflammatory disease.
We carry out translational research directed at understanding molecular mechanisms of action for diseases such as SLE and Sjögren’s syndrome, as well as for children of mothers with these diseases, where the children are at risk of developing congenital heart block due to specific immune reactions.
By identifying these immune reactions and developing new diagnostic methods, it may become possible to prevent development of congenital heart block through prenatal treatment. Clinical research aimed at understanding why inflamed muscles in myositis become weak has led to better diagnostic methods and improved methods of treating myositis both with drugs and with physical therapy and exercise. Clinical research involving drug trials and structured follow-up of new drugs in clinical practice has contributed to the development of a new effective RAS therapy that has been put into clinical use, as well as to the evaluation of the safety and cost-effectiveness of these drugs.
More information can be found in these important scientific articles:
1. Klareskog L et al. Therapeutic effect of the combination of etanercept and methotrexate compared with each treatment alone in patients with rheumatoid arthritis: double-blind randomised controlled trial. Lancet. 2004 Feb 28, 363 (9410):675-81. 2.
2. Padyukov L et al. A gene-environment interaction Between Smoking and Shared Epitope Genes in HLA-DR Provides a High Risk for Seropositive Rheumatoid Arthritis Rheum,2004, 50:3085-92.
3. Salomonsson S, Dörner T, Theander E, Bremme K, Larsson P, Wahren-Herlenius M. A Serologic Marker for Fetal Risk of Congenital Heart Block. Arthritis Rheum, 2003, 46:1233 – 1241.