“…Physiologically, extracellular disturbances in barrier tissues, for instance, caused by the interaction with bacteria and fungi, initiate type 3 response, where interleukin (IL)-17 and IL-22 orchestrate cellular compartments to protect the body against the damage with the aim of restoring tissue homoeostasis [ 6 ]. However, when abnormal, they contribute to SpA pathogenesis by amplifying T helper 17 cells (Th17) response, hence recruiting and activating neutrophils at different disease sites (enthesis, joint, gut, eye, and skin) in a positive loop, further amplified by neutrophilic production of pro-inflammatory mediators, such as IL-23 [ 8 ]. Hereby neutrophils are emerging as pivotal cells in SpA development, being involved in several manifestations, especially in the very early phase of the disease ( Figure 1 ).…”