이미퀴모드로 유발된 건선양 쥐 모델

Abstract

Psoriasis is a chronic inflammatory skin disease affecting 1-2% of the population. The pathogenesis of psoriasis is not fully understood, but recent progress in studying its complex mechanisms revealed that crosstalk among T cells, epidermal keratinocytes, dendritic cells (DCs), neutrophils, endothelial cells and fibroblasts, together with growth factors, chemokines, and cytokines, are important in the development and maintenance of the disease. Recently, much progress has been made in understanding the pathophysiology of psoriasis. But this progress has been hindered by the lack of an appropriate animal model for psoriasis. There have been a large number of genetically engineered (transgenic or knockout) or induced (by immune transfer or by xenotransplantation) murine models for psoriasis. These models exhibit skin conditions that are similar to psoriasis in humans, and each model has its strong points, but many discrepancies exist between mouse skin and human skin. One of the representative psoriatic mouse models is the xenograft model, which uses human psoriatic skin transplanted onto immunodeficient mice. It is a very close approximation of psoriasis in humans in terms of genetic, phenotypic, and immunologic changes, but is expensive and time-consuming and requires specialized laboratory skills. Recently, imiquimod (IQM)-induced psoriasis-like cutaneous inflammation has been reported in mice and humans. IQM is a ligand for toll-like receptor 7 (TLR7) and TLR8 and is a potent immune activator. This mouse model showed similar clinical and immunological changes to human psoriasis. There have been some research to find the exact pathogenesis and progress of this mouse model to help better understanding and inspiration for study and treatment of psoriasis. In this review, the current issues about this model will be provided.