Interleukin-36 as the central amplifier of neutrophilic inflammation: lessons from spatiotemporal transcriptomics in Sweet syndrome

This letter highlights recent mechanistic insights into Sweet syndrome, focusing on the IL-36–PADI4 inflammatory circuit that links neutrophil activation, NETosis and keratinocyte signalling. We discuss how these findings redefine the immunopathogenesis of neutrophilic dermatoses and identify remaining challenges in translating IL-36-targeted therapies to clinical practice.