Psoriasis and Psoriatic Arthritis

Psoriasis is a chronic, immune-mediated skin disease affecting approximately 2–3% of the global population. It is characterized by erythematous, scaly plaques resulting from hyperproliferation and altered differentiation of keratinocytes, accompanied by a pronounced inflammatory response. The disease is driven by complex interactions between innate and adaptive immune pathways, prominently involving IL-17, IL-23, and TNF signaling.

Up to 30% of individuals with psoriasis develop psoriatic arthritis (PsA), a related inflammatory joint disease marked by enthesitis, dactylitis, and progressive joint damage. PsA shares common immune mechanisms with psoriasis but presents additional challenges due to joint involvement and its variable clinical manifestations.

At Redoxis, we offer in vivo and in vitro models relevant to psoriasis and psoriatic arthritis, supporting preclinical evaluation of therapeutic strategies targeting cytokine signaling, T cell activity, and keratinocyte function. Our models allow for assessment of both cutaneous and joint inflammation, histopathological changes, and systemic immune responses.

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 reproducible model of psoriatic arthritis induced by intraperitoneal injection of mannan, a fungal β-glucan derived from Saccharomyces cerevisiae, in Ncf1-mutated mice. Disease onset typically occurs within a few days and is characterized by peripheral joint inflammation, enthesitis, and psoriasis-like skin manifestations, particularly affecting the paws, tail, and ears.

The model closely resembles key clinical and immunological features of human psoriatic arthritis. Disease development is driven by innate immune activation resulting from impaired reactive oxygen species (ROS) production caused by the Ncf1 mutation, leading to dysregulated IL-23/IL-17 signaling and chronic inflammation. The model does not require adjuvants or antigen-specific immunization, making it well suited for studying the interplay between innate and adaptive immune responses.

Disease pathology is mediated by IL-17-producing T cells together with innate immune cells, with critical involvement of the IL-23, IL-17A, and GM-CSF pathways. Draining lymph nodes and spleen can be collected for ex vivo analyses, including immune cell phenotyping, cytokine profiling, and functional restimulation assays, providing valuable mechanistic insights alongside in vivo efficacy studies.

Key Features:

  • Reproducible model of psoriatic arthritis in Ncf1-mutated mice
  • Induced by intraperitoneal injection of mannan
  • Develops peripheral arthritis, enthesitis, and psoriasis-like skin inflammation
  • Driven by dysregulated innate immunity and IL-23/IL-17 signaling
  • Strong involvement of Th17 cells and innate immune populations
  • Compatible with ex vivo immune profiling from lymphoid tissues
  • Suitable for evaluating biologics, antibodies, and small molecules targeting inflammatory 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.

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Inquiries? Questions?

Nina Woodworth

COO