Abstract
In psoriasis (PSO) and atopic dermatitis (AD), the complex inflammatory milieu drives epidermal disease hallmarks that are associated to skin inflammation. The current lack in understanding on how this, often patient-specific, inflammatory signature translates to disease endotypes hampers the development of translational models and the personalized use of targeted drugs. We aimed to identify optimal cytokine combinations to mimic disease phenotypes in human epidermal equivalents (HEEs) and to unravel which disease hallmarks are attributed to specific disease-associated cytokines.
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