Psoriasis and Psoriatic Arthritis

The Imiquimod (IMQ)-induced model is a widely used, acute mouse model of psoriasis-like skin inflammation. It is based on topical application of Aldara™ cream (5% IMQ) on shaved dorsal skin or ears of mice, typically over 5–7 consecutive days.

IMQ is a TLR7/8 agonist that triggers a rapid and robust inflammatory response, mimicking several features of human plaque psoriasis—including epidermal hyperplasia, scaling, erythema, and infiltration of immune cells such as neutrophils, dendritic cells, and Th17 cells.

The model is highly responsive to inhibitors of the IL-23/IL-17 axis and has become a standard tool for screening novel anti-psoriatic compounds and evaluating early immune mechanisms in cutaneous inflammation.

Key Features:

• Acute, reproducible model of psoriasis-like skin inflammation
• Induced by topical application of IMQ on dorsal skin or ear
• Rapid onset of erythema, thickening, scaling, and immune infiltration
• IL-23/IL-17 axis-dependent; responsive to biologics and small molecule inhibitors
• Suitable for histology, cytokine analysis, and scoring of erythema and thickness
• Can be used with knockout or transgenic mice for mechanistic studies

This model is ideal for short-term screening of anti-inflammatory and immune-modulating compounds targeting innate and adaptive pathways involved in psoriasis.

The Mannan-Induced Psoriatic Arthritis (MIP) model is a robust and spontaneous model of psoriatic arthritis induced in SKG mice by intraperitoneal injection of mannan, a fungal β-glucan component derived from Saccharomyces cerevisiae. Disease onset typically occurs within a few days and is characterized by joint inflammation, enthesitis, and psoriasis-like skin changes, particularly on the tail and ears.

The MIP model closely mimics the human psoriatic arthritis phenotype, with joint swelling, dactylitis-like features, and skin involvement driven by dysregulated IL-17 and IL-23 axis signaling. It does not require adjuvants or exogenous peptides, making it ideal for studying innate immune activation and the downstream effects on adaptive immunity.

Disease is primarily mediated by CD4⁺ T cells, particularly Th17 cells, and is dependent on IL-23, IL-17A, and GM-CSF pathways. Lymph nodes and spleen can be harvested for ex vivo restimulation assays, allowing for assessment of antigen-specific T cell responses and cytokine release (e.g., IL-17A, IL-22, IFN-γ). These readouts are valuable for profiling compound effects on immune modulation prior to or in parallel with in vivo studies.

Key Features:

• Spontaneous and reproducible model of psoriatic arthritis
• Induced by intraperitoneal mannan injection in SKG mice
• Displays joint inflammation, enthesitis, and psoriasis-like skin lesions
• Driven by IL-17A, IL-23, and GM-CSF signaling pathways
• CD4⁺ T cell-mediated; strong Th17 involvement
• Compatible with ex vivo restimulation assays from draining lymph nodes and spleen
• Suitable for testing biologics and small molecules targeting innate and adaptive immune pathways

This model offers high translational relevance for psoriatic arthritis research, especially for therapies targeting IL-23/IL-17 axis and Th17-driven inflammation in both skin and joints.