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New breakthrough drug shows promise to fight arthritis

Patients crippled by rheumatoid arthritis have been given new hope after the discovery of a protein which triggers the disease

London Daily Express—July 1, 2013

Powerful new drugs to help the 350,000 sufferers in Britain are a step closer after the breakthrough, giving a "completely new angleG" to treatment.

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.

Researchers at 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 signaling 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.

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.

Dr Carl Blobel from HSS said: "When we tested mice that don't have IRHOM2 in a model for inflammatory arthritis, we found they were protected and they were protected as well as mice that didn't have any TNF. Because TNF is the driver of rheumatoid arthritis in human disease, as evidenced by how well anti-TNF drugs work, we feel that this provides a new angle on blocking TNF release."

The researchers will next identify safe antibodies or drug compounds that block the IRHOM2 function.

Dr Salmon said: "In theory, IRHOM2-targeted drugs will have less toxicity than TNF alpha blockers."

This story originally appeared at express.co.uk.


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