作者: Daniele Mauro , Federica Macaluso , Serena Fasano , Riccardo Alessandro , Francesco Ciccia
DOI: 10.1007/S11926-019-0834-9
关键词:
摘要: A growing body of evidence supports the relevance interleukin-23/interleukin-17 (IL-23/IL-17) pathway for pathogenesis axial spondyloarthritis (axSpA) and its treatment. Recently, innate lymphoid cells (ILC), a heterogeneous family immune effector cells, have been identified as relevant contributor in tissue homeostasis, partially via IL-23/IL-17 axis. This review describes biology origins group 3 ILCs (ILC3s) humans, focusing on their role axSpA. Clinical trials showed effectiveness IL23/IL-17 axis inhibition both (SpA) Inflammatory Bowel Disease (IBD). Recent findings confirm high prevalence subclinical gut inflammation patients with SpA. Translational data humans demonstrated an increase number ILC3s responsive to IL-23 producing either IL-22 or IL-17 SpA patients. The observation gut-derived circulation at inflamed tissues suggest recirculation from mucosal site possibly enthesis joints. Multiple observations demonstrate expansion IL-17- IL-22-producing ILC3 subclinically These also observed normal entheses, seem be able re-circulate patients, thus contributing disease perpetuation. development tools that can provide access diseased sacroiliac joint spinal entheses will valuable knowledge axSpA pathogenesis.