The drugs he and his colleagues developed for arthritis had already proved successful against other autoimmune diseases, Professor Marc Feldmann told the 2008 Congress of European Pharmacological Societies (EPHAR), held at Manchester.
The immune system is the body's front line of defence against disease-causing invaders such as bacteria, viruses and parasites.
However, sometimes this formidable defender can turn against us - mistakenly attacking and damaging the body's own tissues. This case of mistaken identity is the cause of common autoimmune diseases such as type one diabetes, rheumatoid arthritis and lupus.
Feldmann said, "In autoimmune diseases, such as arthritis, we discovered that cytokines (protein messaging molecules) are over-produced causing the immune system to fight itself, resulting in inflammation and tissue destruction."
"We further found that by blocking just one cytokine - Tumor Necrosis Factor (TNF) alpha - we were able to block all the cytokines involved in the inflammation, with remarkable clinical results."
His team's research led to the development of three anti-TNF alpha drugs - infliximab, etanercept and adalimumab - which have had a dramatic effect on the symptoms of rheumatoid arthritis patients, protecting the joints from further deterioration in the vast majority of cases.
Blocking TNF alpha has had further success in treating several more chronic inflammatory conditions, including Crohn's disease, psoriasis, psoriatic arthritis, ankylosing spondylitis and ulcerative colitis.
But Professor Feldmann, Head of the Kennedy Institute of Rheumatology, believes similar drugs have the potential to treat many other medical conditions, particularly on arthosclerosis.
His work with his colleague Dr Claudia Monaco has resulted in the emergence of a new branch of medicine - anti-cytokine therapy - and research elsewhere has showed promise in yet more conditions, including the potentially fatal acute alcoholic hepatitis.
Professor Feldmann had said on the eve of the conference: "During the conference I will be discussing the potential therapeutic targets in tissue affected by atherosclerosis, which is caused by a chronic inflammatory response in the walls of the arteries, in large part, caused by an excessive immune response to cholesterol.
"I will also discuss whether it is possible - even likely - that cytokines play a critical role in all diseases involving multiple biological processes, thus providing therapeutic targets for all unmet medical needs."