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Rheumatoid arthritis is a chronic disabling disease affecting at least 1% of the population on a worldwide basis. Research aimed at understanding the pathogenesis of this disease led to the identification of TNFalpha as a major pro-inflammatory cytokine expressed in the inflamed joints of patients with rheumatoid arthritis. Subsequently, in vitro studies provided evidence to suggest that TNFalpha played an important role in driving the expression of additional pro-inflammatory cytokines, such as IL-1, GM-CSF, IL-6, and IL-8, in synovial cell cultures. Another important finding that confirmed the pathological significance of TNFalpha was that mice genetically engineered to overexpress TNFalpha spontaneously developed arthritis. Subsequently, the therapeutic effect TNFalpha blockade was tested in animal models prior to clinical trials in human patients, which provided unequivocal verification of the validity of TNFalpha as a therapeutic target. Anti-TNFalpha therapy is now accepted as a fully-validated treatment modality for rheumatoid arthritis.


Journal article


Ernst Schering Found Symp Proc

Publication Date



107 - 130


Animals, Arthritis, Rheumatoid, Cell Movement, Cytokines, Estrogens, Humans, Neovascularization, Physiologic, RNA, Messenger, T-Lymphocytes, Tumor Necrosis Factor-alpha