FRIDAY, July 24, 2026 (HealthDay News) -- Elevation of interferon (IFN)α drives an immune endotype of Sjögren disease, according to a study published in the August issue of The Lancet Rheumatology.
Deborah Forbes, M.B.Ch.B., from the University of Edinburgh in the United Kingdom, and colleagues used data from the U.K. Primary Sjögren's Syndrome Registry (UKPSSR) and U.K. Biobank to examine the role of IFNα in Sjögren disease.
A total of 177 people with Sjögren disease were identified in the UKPSSR between Aug. 1, 2009, and March 31, 2012. In addition, 47,606 people without Sjögren disease and 257 with Sjögren disease were identified in the U.K. Biobank Pharma Proteomics Project between March 13, 2006, and Oct. 1, 2010, including 137 individuals sampled before diagnosis. The researchers found that 61 percent of people with Sjögren disease in the UKPSSR had elevated IFNα concentrations. In the U.K. Biobank Pharma Proteomics Project, oligoprotein IFN signatures were detected up to 14 years before Sjögren disease diagnosis. A distinct immunological endotype, characterized by cytopenia, hypergammaglobulinemia, multiple autoantibodies, and autoimmunity against the Sjögren autoantigen TRIM21/ Ro52 was seen in individuals in the UKPSSR with elevated IFNα. The key features of the endotype were recapitulated in a mouse model of systemic chronic IFNα elevation, in which IFNα4 was overexpressed by conventional dendritic cells; these could be partially reversed by blockade of the type 1 IFN receptor.
"We are delighted to have shown how precision medicine technologies can be used in Sjögren's disease to help decode the immune pathways which cause disease," coauthor David Hunt, Ph.D., also from the University of Edinburgh, said in a statement.
Several authors disclosed ties to the biopharmaceutical industry; one author disclosed ties to the publishing industry.
