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Professor Ehrenstein’s specialism is rheumatoid arthritis and he said: “Because we are becoming much better at targeting our treatments, we are much better at suppressing symptoms. We do not have a cure for rheumatoid arthritis yet but it’s something that people are working towards.”

Among work being done is that by a team at the La Jolla Institute for Allergy and Immunology in California in the United States, who recently revealed that they had developed a potential new treatment. Working in collaboration with colleagues at the University of California, San Diego, they came up with a drug that focuses on the cells that are directly responsible for the cartilage damage in affected joints. Rheumatoid arthritis, an autoimmune disease that leads to stiff, deformed joints and often crippling pain, affects millions of people across the planet as the immune system attacks the body’s own tissue. The inflammatory processes activate synoviocytes (FLS), cells that line the inside of joints. Once mobilised, the FLS invade the surrounding cartilage and secrete enzymes that break down the firm, rubbery tissue that cushions the bone. In addition, they trigger bone destruction.

Much of the current treatment focuses on intercepting the immune system’s misdirected attack on the lining of affected joints to alleviate the symptoms, reduce inflammation and slow the progression of the disease. For the study’s lead author Nunzio Bottini, M.D. Ph.D., associate professor at La Jolla Institute and associate professor of Medicine at the University of California, San Diego, better understanding immunology is the key to advancement. He said: “Unfortunately, for around 40 per cent of patients, immune-targeted therapies are not sufficient to bring them into full remission. If we could add a drug that acts on a different target without increasing immune suppression it could be very valuable.

“Even if your inflammation is completely under control with the help of current therapies – and they are excellent – the damage to the skeletal structure is not necessarily arrested in the long term because synoviocytes continue to cause damage and, although synoviocytes are considered the main effectors of cartilage damage in rheumatoid arthritis, there’s no therapy directed against them.”

That was until post-doctoral researcher and first author, Karen M. Doody, Ph.D., while screening samples from rheumatoid arthritis patients, discovered that an enzyme known as RPTPσ, short for receptor protein tyrosine phosphatase sigma, is highly expressed on the surface of FLS. Normally, RPTPσ is kept inactive but, when activated using a biological decoy, it weakens the ability of arthritic synoviocytes to aggressively invade the joint’s cartilage. Co-author Gary S. Firestein, M.D., dean and associate vice chancellor of Translational Medicine and director of the Clinical and Translational Research Institute at UCSD, said: “The unique aspect of this approach is the ability to improve symptoms and decrease joint damage while potentially avoiding any negative effects on normal immune responses and susceptibility to infections.”