Breakthrough Study Identifies Cellular Source of Inflammation in Spondyloarthritis

Recent research conducted by NDORMS at the University of Oxford has uncovered a crucial aspect of the inflammatory process in spondyloarthritis (SpA), a chronic autoimmune condition affecting the spine and joints. The study reveals that CD4+ tissue-resident memory Th17 (TRM17) cells are the primary producers of interleukin-17 (IL-17), a key inflammatory protein that drives joint inflammation in SpA. This discovery challenges previous assumptions that circulating Th17 cells or innate immune cells were the main sources of IL-17 in inflamed joints. According to Dr. Liye Chen, the senior author of the study, identifying these TRM17 cells as the main source opens up new avenues for targeted therapies aimed at the cellular drivers of inflammation.

The research employed advanced techniques such as single-cell RNA sequencing and spatial transcriptomics to analyze synovial tissue samples from patients with axial SpA and psoriatic arthritis. The findings demonstrate that TRM17 cells remain within joint tissues and sustain inflammation over time, unlike their circulating counterparts. This insight suggests that current IL-17-blocking treatments, which benefit about half of SpA patients, could be made more effective by focusing on eliminating or modulating these resident cellular factories of IL-17. Such targeted approaches hold the potential for long-lasting control of joint inflammation without continuous medication.

Prof Holm Uhlig from the Oxford-J&J Cartography Collaboration highlighted the importance of applying cellular mapping technologies to uncover drivers of disease and develop precision medicine strategies. The study’s results underscore the significance of understanding specific cellular contributors to immune-mediated diseases, paving the way for innovative treatment options that could transform patient outcomes.

Source: https://medicalxpress.com/news/2025-06-key-driver-inflammation-spondyloarthritis.html