Genetic influences on susceptibility to and clinical course of rheumatoid arthritis have been known for a long time, but have so far eluded systematic, genome-wide analysis. In recent years, the availability of new typing techniques and international consortia with large patient cohorts has generated a wealth of new information on the genetic basis of this autoimmune disease. Newly described associations between immunologically relevant gene polymorphisms and RA susceptibility have already been replicated with great statistical power, and are currently incorporated into new, pathogenetically relevant functional pathways. The resulting new concepts identify cell populations of great potential relevance for the pathogenesis of the disease, and ultimately might lead to new diagnostic and therapeutic approaches in RA.
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