Powerful new drugs to help the 350,000 sufferers in Britain are a step closer after the breakthrough, giving a “completely new angle” to treatment.
The finding could revolutionise care for the devastating condition and scientists in America are already developing pills.
Researchers say it could lead to an effective and potentially less toxic alternative therapy to drugs which are currently prescribed to arthritis patients.
Around a third of people do not respond to or cannot tolerate treatment at the moment.
Although the drugs have improved care over the past decade they suppress the immune system, leaving patients at risk of developing infections.
Dr Jane Salmon, who led the study, said: “We have identified a clinically relevant target that can be applied to patients in the near term.”
The discovery means a new “gateway” for treatment, leading to an effective and potentially less toxic alternative therapy to the current anti-TNF (tumour necrosis factor) drugs.
More than 10million people in the UK suffer from arthritis, which causes crippling pain and inflammation within a joint. Many are in constant agony.
Researchers at the Hospital for Special Surgery in New York City, have found a potential new target for drugs to treat patients, the protein called IRHOM2.
Rheumatoid arthritis (RA) is an autoimmune disease which is triggered largely by TNF-alpha, a small signalling protein usually involved in launching a protective inflammatory response in the body.
But with excessive TNF production, immune cells can become activated inappropriately and cause tissue inflammation, producing diseases such as RA.
While TNF-blockers help many RA patients, these treatments are very expensive and not all benefit.
RA is notoriously difficult to treat because it is caused by a malfunctioning immune system. In healthy people the immune system fights infection, but in conditions such as RA it attacks body tissue and causes inflammation.
The research – published online in the Journal of Clinical Investigation – set out to determine whether blocking IRHOM2 could be a strategy to treat RA.
They used a model that mimics human rheumatoid arthritis in mice genetically engineered to be deficient in IRHOM2. The rodents did not develop inflammatory arthritis.