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.