Gene is identified that regulates tissue damage in rheumatoid arthritis
A gene that seems to play a vital role in regulating the severity of tissue damage experienced by people with rheumatoid arthritis has been identified by teams from University College Dublin and the University of Sheffield.
By analysing DNA and biopsy samples from the joints of over 1,000 people with rheumatoid arthritis, the team managed to identify the importance of a particular protein called C5orf30 in disease progression.
This protein was highly expressed in rheumatoid arthritis synovial fibroblasts, which is the type of cell implicated in joint damage. Inhibition of C5orf30 accentuated tissue damage and joint inflammation. The findings mean it could become easier to monitor people at greatest risk of severe forms of rheumatoid arthritis.
“Our findings provide a genetic marker that could be used to identify those rheumatoid arthritis patients who require more aggressive treatments or personalised medicine,” explains study lead, Prof Gerry Wilson. “They also point to the possibility that increasing the levels of C5orf30 in the joints might be a novel method of reducing tissue damage caused by rheumatoid arthritis.”
A spokesperson from Arthritis Research UK comments:
“Although anti-TNF and other biological therapies are effective in about 70% of patients with inflammatory arthritis, they don’t work for everyone. At the moment we have no way of predicting which patients will respond to which therapy, or who will develop the most severe form of the disease, so drugs are prescribed on a trial and error basis.
“For us and other research bodies, identifying blood or tissue markers that help to target the right drug to the right patient at the right time; so-called stratified or personalised medicine is a priority area and something we are investing in heavily.
“The new findings from this group could take us a step closer to that goal by finding a genetic marker that could predict who will develop the severest symptoms so that patients can be given drugs we know will work for them early in their disease that will prevent or minimise joint damage.”
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Image credit: Johannes Ahlmann
