title: Anti-TNF therapy, from rationale to standard of care: what lessons has it taught us?
abstract: In the mid-1980s, new molecular tools enabled the biology of cytokine expression and regulation to be studied. Our group uncovered a TNF-dependent cascade in active rheumatoid synovium, suggesting that TNF might be a therapeutic target; this concept was supported in an animal model of the disease. The proof of concept was a series of clinical trials, which have led to marked changes in the therapy of human rheumatoid arthritis and subsequently of other diseases. The work with TNF clearly demonstrated the importance of cytokines in medicine as well as the capacity of mAbs (or receptor fusion proteins) to be used long-term in large populations, thus changing the therapeutic landscape.
authors.affiliation: Kennedy Institute of Rheumatology, Imperial College, London, United Kingdom. m.feldmann@imperial.ac.uk
authors.forename: Marc
authors.initials: M
authors.lastname: Feldmann
authors.forename: Ravinder N
authors.initials: RN
authors.lastname: Maini
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D002986:Clinical Trials as Topic; D004359:Drug Therapy, Combination; D006801:Humans; D000069285:Infliximab; D008727:Methotrexate / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D008727:Methotrexate