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Neutrophil-derived IL-26 triggers a self-sustaining loop that drives autoinflammation in psoriasis
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Description
Skin-infiltrating neutrophils release IL-26, which activates keratinocytes to produce neutrophil-recruiting CXCL1 and CXCL8 chemokines along with inflammatory IL-1 cytokines. IL-26 also forms complexes with commensal bacterial DNA present in skin lesions, leading to a continuous activation of neutrophils. The IL-26–driven pathway provides a self-sustaining loop that amplifies neutrophil recruitment, autoinflammation, and leads to the development of pustular disease phenotype.
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