Marc Feldmann MBBS, PhD, FRS

Professor Sir Marc Feldmann is a pre-eminent immunologist at the University of Oxford where he is Head of the Kennedy Institute of Rheumatology and leads the Cytokine and Cellular Biology section. He graduated with an MBBS degree from the University of Melbourne in 1967. After an internship (residency) at St Vincent’s Hospital, he earned a PhD in Immunology in 1972 under the supervision of Sir Gustav Nossal at the Walter and Eliza Hall Institute of Medical Research. He then went to the UK as a CJ Martin Fellow of NHMRC and his career has since progressed in London, initially at the Imperial Cancer Research Fund's Tumour Immunology Unit, then at the Charing Cross Sunley Research Centre and the Kennedy Institute of Rheumatology which joined with the Faculty of Medicine at Imperial College in 2000, prior to its transfer to the University of Oxford in 2011. Marc Feldmann’s pre-eminence stems from his 1983 publication that provided a new hypothesis for the mechanism of induction of autoimmune diseases and highlighted the role of cytokines. He was awarded the 2007 Curtin Medal for outstanding achievements throughout his career, which have stemmed from this discovery and the subsequent development of therapies improving the quality of life of millions of people worldwide with rheumatoid arthritis.

From 1984 he collaborated with Ravinder (now Sir) Maini at the Kennedy Institute of Rheumatology, studying the disease mechanism in rheumatoid arthritis. They showed that diseased joints have far more pro-inflammatory cytokines than normal, and identified one of these, Tumour Necrosis Factor Alpha, (abbreviated TNFα) as the key. Blocking TNFα with a monoclonal antibody reduced levels of the other pro-inflammatory cytokines in test-tube models of arthritis, and provided the rationale for testing TNF blockade in rheumatoid arthritis patients for whom all existing treatment had failed. This led to the first of a series of successful clinical trials performed in 1992, at Charing Cross Hospital. Several approved antiTNF drugs have now become the therapy of choice for stopping the inflammatory and tissue-destructive pathways of not only rheumatoid arthritis, but other autoimmune diseases including Crohn's disease, ulcerative colitis, ankylosing spondylitis, psoriasis and psoriatic arthritis. These drugs are used extensively, with millions of patients successfully treated worldwide.