Ravinder Maini was born in 1937 to Punjabi Indian parents, the family having emigrated to East Africa. Ravinder spent his childhood in Kampala, Uganda and completed his schooling in London and entered Cambridge University in 1956 for pre-medical followed by clinical studies at Guy’s Hospital, London. Ravinder undertook training in Internal Medicine and Rheumatology in London and a Fellowship in Immunology. From 1970 he combined clinical practice and research as a clinician-scientist throughout his career. His research initially prioritised studies into the role of humoral and cellular mechanisms, and possible role of infections in pathogenesis and aetiology of rheumatoid arthritis (RA). From 1985 onwards, together with Marc Feldmann, Ravinder led a team of scientists and clinicians that identified Tumour Necrosis Factor as a key regulator of the proinflammatory cytokines implicated in the pathogenesis of RA. In collaboration with a Biotech company and international collaborators, clinical trials demonstrated the first safe and effective therapy by an anti-TNF monoclonal antibody, now a standard treatment. Experimental studies provided insight into the mechanisms of action. Maini and Feldmann have been jointly awarded international prizes for their research, including the Crafoord Prize, The Lasker prize for Clinical Research, and The Canada Gairdner International Award.

Research Interests

As a physician scientist my research interest is in understanding molecular mechanisms underlying autoimmune rheumatic diseases and applying the knowledge gained to improving the health of patients with these common disabling diseases. At the beginning of my scientific career in 1968, the aetiology and pathogenesis of these disorders was obscure but it was becoming clear that immunity and inflammation played a part. The characterisation of cytokines at the protein and DNA level in the early 1980s and their availability as tools focussed my research into investigating their role in the biology and pathogenesis of rheumatoid arthritis (RA). In collaborative studies with Marc Feldmann using patient derived cell culture and vivo animal models the concept was established that TNF alpha played a key role in inflammation and joint damage observed in RA. In seminal clinical trials the efficacy of TNF blockade by a specific anti-TNF antibody, augmented by co-therapy with low dose methotrexate, was established and is now widely applied as a standard of care for RA. In mechanism of action studies TNF blockade was shown to impact on immune cell recruitment and angiogenesis by down regulating several cytokines, chemokines and adhesion molecules. Understanding why disease remission is rarely achieved remains a challenge for future research.

Membership Type

International Member

Election Year


Primary Section

Section 43: Immunology and Inflammation