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The main focus of our group is Rheumatoid arthritis, but our research has a strong relevance also for ankylosing spondylitis, psoriatic arthritis and other chronic inflammatory diseases. Taken together these diseases affect about 2 % of the population, and if they are not treated, they may lead to disability and joint destruction in most affected individuals.



Our research is aimed at understanding how environment/lifestyle interacts with genes, in giving rise to immune and inflammatory reactions that may cause arthritis. From a detailed understanding of these factors in different distinct subsets of arthritis disease, we will increasingly be able to prevent and treat patients based on knowledge of the specific disease-causing mechanisms active in that particular individual. We will also be able to advice healthy individuals (such as family members of these suffering from arthritis) a on preventive measures against arthritis.

Detailed molecular studies on immune reactions that cause arthritis in different genetic contexts are performed in the various research teams in CMM, with Leonid Padyukov being responsible for genetics, Vivianne Malmström for cellular immunology, Anca Catrina for studies of mode of action of anti-rheumatic therapies, and Jon Lampa for studies on interactions between the brain and the immune system in arthritis.. We also have a close collaboration with epidemiology temas led by Laprof Lars Alfredson and Johna Askling as well as with our clinical trials and treatment Unit at Karolinska, led by Prof Ronald van Vollenhoven.

Our group has a leading edge in the world concerning research aimed at understanding how genes, environment and immunity interact in causing disease. Thus, we use our large longitudinally followed patient cohorts as well as our control populations to perform detailed genetic studies on susceptibility genes. We use knowledge of methods to analyze gene-environment interactions describe such interactions in RA, and we use immunological studies to understand the fine specificity of immune reactions against citrullinated proteins/peptides and other autoantigenes that may be responsible for disease development in different subsets of RA.

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