Hopes of breakthrough for psoriatic arthritis patients after Sanger Institute and Oxford University discovery
A third of patients with the skin condition psoriasis develop psoriatic arthritis, for which are some treatments but no cure.
The long-term condition, which causes affected joints to become swollen, stiff and painful, can worsen over time. In the worst cases, it can permanently damage joints, meaning surgery is required.
But there was new hope for those with the condition on Monday, when a study was published showing psoriatic arthritis may be activated by the same trigger in different patients.
The research by the Wellcome Sanger Institute and University of Oxford gives the strongest evidence yet of a single cause for the disease after identifying high levels of a specific receptor in immune cells from patients.
It could help scientists find the exact molecular trigger, which would raise hopes of finding a targeted treatment.
The researchers used single cell technology and machine learning to analyse thousands of individual immune cells from fluid drained from the knees of patients with psoriatic arthritis.
Dr Hussein Al-Mossawi, honorary research associate at the Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS) at the University of Oxford, said: “Our data suggest that psoriatic arthritis doesn’t just appear out of nowhere. Each receptor is like a unique lock that recognises a molecular key and we discovered, that across the patients, they are recognising a common molecule.
“This gives the first evidence that the T cells are seeing and reacting to the same molecule, which acts as a trigger for the disease. We don’t know the exact culprit yet, but this is a great step forward in understanding the disease.”
Dr Sam Behjati, group leader and Wellcome Trust intermediate clinical fellow at the Wellcome Sanger Institute , said: “Our study produced the largest single cell dataset from psoriatic arthritis patients to date.
“It is helping us to understand the intricate mechanisms behind psoriatic arthritis, including starting to unravel the signals that tell the T cells to cross over into the joint fluid. Imagine the cells as train passengers with a ticket that tells them at which station to get off - the single cell data is allowing us to read that destination for each cell, and understand the signals.”
Paul Bowness, professor of experimental rheumatology at NDORMS said: “Our findings indicate that specific T cells are likely to be targeted to enter the joint, where they are triggered to expand, creating inflammation and causing psoriatic arthritis.
“The next stage of research will be to find the key that is unlocking the disease in patients - from the signals that direct cells to the joint, to what then triggers them to expand. If we can understand these, we could move towards creating therapies that would prevent this, potentially providing a cure.”