Injury, dysbiosis and filaggrin deficiency drive skin inflammation via keratinocyte IL-1 α release

Our data demonstrate that injury and dysbiosis drive intracellular IL-1 α release from keratinocytes to mediate chronic inflammation in filaggrin-deficient mice. IL-1α and dysbiosis could represent therapeutic targets to reduce skin inflammation in atopic dermatitis. (Source: Journal of Allergy and Clinical Immunology)

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