Abstract
Psoriasis is a common chronic skin disease characterized by a pro-inflammatory environment mediated by keratinocytes and both innate and adaptative immune responses. This inflammation is mostly driven by the IL-17/IL-23 axis resulting in the production of inflammatory and immune factors (chemokines and antimicrobial peptides) by keratinocytes. These mediators lead to an amplification loop and consequently to an epidermal hyperplasia. To our knowledge, very few 3D skin models involving lymphocyte T-helper cell type 17 (LTh17) reproduce accurately psoriasis features.
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