Over half of patients with Sjögren’s disease – when the immune system mistakenly attacks the body’s moisture-producing glands – have chronically high levels of an inflammatory protein called interferon alpha (IFN-α), identifiable long before symptoms develop.
Pinpointing the involvement of IFN-α could help doctors target the right treatment to the right patient, improving management of the condition, experts say.
Overlooked condition
Sjögren’s disease affects around half a million people in the UK. 90 per cent of adults diagnosed with the condition are women.
The disease affects the exocrine glands – which make and release substances like tears and saliva – and other organs, causing chronic inflammation and preventing them from working properly.
There is currently no cure, so treatment focuses on managing symptoms, which can include dry eyes and mouth, joint pain and extreme tiredness.
Sensitive test
Scientists from the University of Edinburgh and University Bonn in Germany studied the immune system of over 170 women and men with Sjögren’s disease. The body normally only produces IFN-α in tiny quantities, so researchers used a new, ultra-sensitive method to detect individual molecules.
Around 60 per cent of patients had an increased amount of IFN-α. This was linked to different activity levels of certain genes involved in the immune system, leading to a unique fingerprint of proteins in the blood of this group of patients.
Researchers extended their findings using data from the blood samples of 250 patients diagnosed with Sjögren’s disease in the UK Biobank. Analysis of the samples showed that IFN-α fingerprints could be detected in blood more than ten years before patients developed the disease.
The research team were also able to show that mice which produce high levels of IFN-α developed features of Sjögren’s disease, and responded to a drug which blocked the biological effects of IFN-α.
Two pathways
The findings suggest that there are two distinct pathways linked to the development of Sjögren’s disease. This so-called immune diversity could support the use of treatments to suppress IFN-α specifically for patients with high levels of the protein, experts say.
It could also offer a route for the development of potential new treatments among this subset of patients, as well as predicting disease, they add.