Interleukin 23 is Critical in the Pathogenesis of Spondyloarthropathy and Acts on A Novel Population of Interleukin 23r+entheseal Resident Cells

Spondyloarthropathy is characterised by inflammation, bone erosion, and new bone formation at the entheseal insertions of tendons and ligaments to bone. Lack of understanding of the underlying mechanisms that drive entheseal disease has seriously inhibited design of therapeutics. Although anti-tumour necrosis factor (TNF) therapy reduces signs and symptoms of inflammation, residual inflammation continues and bone growth is not inhibited. This suggests that TNF is not the optimum target to modify entheseal disease.