A Review on: Induction Models of Psoriasis

Abstract

Psoriasis is a chronic, immune-mediated inflammatory skin disorder characterized by keratinocyte hyperproliferation, inflammation, and immune dysregulation. To understand its pathogenesis and evaluate potential therapies, various preclinical models of psoriasis have been developed. These models include the UV-B-induced model, genetically engineered models, and chemically induced models, each replicating specific aspects of psoriasis pathology. The UV-B-induced model closely mimics the inflammatory response, keratinocyte hyperproliferation, and immune activation seen in human psoriasis, though it primarily represents acute inflammation and does not fully capture the chronic, relapsing nature of the disease. Genetically engineered models, such as the K14-Stat3 and IL-23 injection models, provide deeper insights into the molecular mechanisms of psoriasis, particularly the IL-23/IL-17 axis, but are limited by their inability to fully replicate immune dysregulation and chronic disease progression. Chemically induced models like the TPA and Oxazolone models allow for focused studies on specific immune pathways, while xenograft models using human tissue offer a more human-relevant context for studying immune cell interactions and testing therapies. While each model has its limitations, together they provide comprehensive tools for advancing psoriasis research, investigating immune mechanisms, and developing effective therapeutic strategies.