This link between IL-23 responsive cells and initiation of disease in animal models direct further in depth characterization of both innate and adaptive immune cells from the moment of triggering of inflammation (possibly in the pre-clinical disease stage) to onset of clinically manifest spondyloarthritis to further elucidate which IL-23 responsive cells drive pro-inflammatory cytokine production, including IL-17A, and which cells drive IL-17 production independently of IL-23. The gene discussed is IL37; the disease is spondyloarthropathy.