The importance of neutrophil-keratinocyte crosstalk in early psoriasis pathogenesis was highlighted by a recent report [49], in which the anti-IL-17A antibody secukinumab caused a rapid reduction in cutaneous neutrophils alongside histological improvement in keratinocyte abnormalities and downregulation of keratinocyte-derived neutrophil chemoattractants e.g. CXCL1. Here, CXCL1 is linked to psoriasis.