Scientists have pinpointed the cause of a debilitating back problem that affects thousands, leading to hope that it could pave the way for new treatments.
Until now the exact driver of axial spondyloarthritis (SpA) – a form of chronic inflammatory arthritis – has not been known.
Experts knew that patients diagnosed with the condition had an abundance of an inflammatory protein known as Interleukin-17 (IL-17) but were unsure why.
Now researchers at Oxford University alongside the charity Versus Arthritis have found it is caused by a specific cell found in tissue around joints.
Rather than circulating around the body, the team found that in patients with the condition these cells became trapped in the joints, producing inflammation in the area, which led to SpA.
About 200,000 people in the UK are thought to have axial spondyloarthritis. While it primarily affects the spine, it can also inflame joints elsewhere.
The first symptom is typically back and buttock pain that wakes patients in the night and is worse in the morning.
Those affected often experience fatigue, and are more likely to develop the red, itchy skin condition psoriasis and irritable bowel disease.
Scientists have pinpointed the cause of a debilitating back problem that affects thousands, leading to hope that it could pave the way for new treatments (Stock Photo)
Symptoms usually appear before the age of 45. Experts have previously suggested up to 90 per cent of cases are hereditary.
Over time it can be disabling as it can cause bones in the spine to fuse together.
‘This is a significant step forward,’ said Dr. Liye Chen, Versus Arthritis fellow at Oxford and senior author of the study.
‘We’ve identified CD4+ TRM17 cells as the main source of IL-17 in SpA joints – a previously unrecognised role.’
Experts say the discovery could lead to new treatments for the estimated 50 per cent of patients who do not respond well to current options.
Dr. Chen explained: ‘Current IL-17-blocking therapies benefit about half of SpA patients but require ongoing treatment and rarely lead to lasting remission.
‘By targeting the CD4+ TRM17 cells themselves – the “factories” of IL-17 – we may be able to achieve long-term control of inflammation without continuous medication.’
