C57 mouse imiquimod-induced psoriasis model, IMQ psoriasis animal model, imiquimod cream induced psoriasis vulgaris model, epidermal hyperplasia and skin inflammation model, Th17/IL-23 axis inflammation model, psoriasis drug screening model

The C57 mouse imiquimod cream-induced psoriasis model is the most widely adopted gold-standard acute psoriasis model for basic psoriasis research, pathogenesis exploration and pharmacodynamic evaluation of anti-psoriatic drugs. Imiquimod (IMQ) is a small-molecule immune modulator and Toll-like receptor 7/8 (TLR7/TLR8) agonist. Continuous topical application specifically activates cutaneous innate and adaptive immune pathways, enhances the activity of dendritic cells, keratinocytes and immune cells, and triggers excessive activation of the core IL-23/Th17 inflammatory axis. It markedly elevates the secretion of pro-inflammatory cytokines including IL-17A, IL-22, TNF-α and IL-6. This treatment induces typical pathological changes of psoriasis, such as excessive epidermal hyperplasia, parakeratosis, acanthosis, Munro microabscesses and dense dermal inflammatory infiltration. Meanwhile, macroscopic lesions including erythema, scaling, skin thickening, protuberance and crusting can be observed, which are highly consistent with the histological and immunological characteristics of clinical psoriasis vulgaris. With short modeling cycle, stable phenotypes and excellent reproducibility, this model requires no surgical operation. It is suitable for exploring psoriasis pathogenesis, preclinical screening and mechanistic verification of candidates with anti-inflammation, anti-epidermal hyperplasia and Th17 immune regulation effects, and has been recognized as a classic in vivo evaluation system in global dermatological research.

SPF-grade C57BL/6 mice aged 6–8 weeks with body weight of 18–22 g are used, and male mice are preferred. C57BL/6 mice present high sensitivity to IMQ-induced cutaneous inflammation and epidermal hyperplasia, with uniform IL-23/Th17 inflammatory responses and minor individual differences, which is the standard strain for establishing IMQ-induced psoriasis model. All mice are housed in an SPF barrier system with constant temperature and humidity and 12 h light/dark cycle, and have ad libitum access to food and water. All mice receive 7 days of adaptive sterile feeding before formal experiments. Dust, external stimuli and environmental stress are strictly controlled throughout the experiment to avoid interference with immune response and lesion formation, so as to ensure parallel and stable data among groups.

Modeling Success Criteria

Macroscopic Lesion Scoring (Simplified PASI Score)

Three evaluation items including erythema, scaling and skin thickening are assessed. Each item is scored from 0 to 4 points, and the total score ranges from 0 to 12 points. Score 0 represents normal skin, and score 4 represents the most severe symptoms. Modeling success criteria: The total lesion score of the model group is significantly higher than that of the blank group, with obvious erythema, silvery scaling and skin protuberance and thickening, which confirms successful modeling.

Skin Thickness Measurement

The thickness of the central dorsal lesional skin is measured uniformly by electronic vernier caliper. The skin thickness of the model group is significantly higher than that of the blank group, with obvious abnormal proliferation of stratum corneum and epidermis, which is consistent with the skin hypertrophy characteristics of psoriasis.

Histopathological Characteristics

HE staining of lesional tissues shows typical pathological manifestations of psoriasis: epidermal hyperkeratosis, parakeratosis, Munro microabscesses in stratum corneum, obvious acanthosis and elongated rete ridges. Superficial dermal vasodilation and congestion are observed, accompanied by extensive diffuse infiltration of lymphocytes, neutrophils and monocytes. The above pathological changes are highly consistent with clinical psoriasis vulgaris.

Immunoinflammatory Indexes

The expression levels of Th17-related pro-inflammatory cytokines including IL-17A, IL-22, IL-23, TNF-α and IL-6 in skin tissues and serum of the model group are significantly upregulated, indicating abnormal activation of IL-23/Th17 inflammatory axis, which serves as the core index for evaluating the immunological characteristics of this model.

Model Advantages

As the most widely used acute induced gold-standard model for psoriasis research worldwide, this model has a clear modeling mechanism that specifically activates TLR7/8 and core IL-23/Th17 pathways, which is highly consistent with the mainstream pathogenesis of clinical psoriasis. The total modeling cycle is only 7 days, with simple operation, no surgical trauma and extremely low animal mortality. It presents stable lesions, minor intra-group individual differences and excellent experimental reproducibility. Typical manifestations including macroscopic scaling, erythema, skin thickening, pathological parakeratosis and microabscesses are easy to quantify with significant statistical differences. It is suitable for preliminary screening of topical and oral anti-psoriatic drugs, research on immune regulation and epidermal hyperplasia mechanisms. The experimental data are highly recognized for project application, dissertation and SCI paper publication.

Research Applications

The C57 mouse imiquimod cream-induced psoriasis model is mainly applied to explore the pathogenesis of acute exacerbation of psoriasis vulgaris, regulatory mechanisms of TLR7/8 innate immune pathway and IL-23/Th17 inflammatory axis. It is widely used for pharmacodynamic screening and activity evaluation of topical creams, gels, ointments and oral preparations with effects of anti-erythema, anti-scaling, inhibiting excessive epidermal hyperplasia and blocking Th17 inflammation. It can also be used to verify the targets of traditional Chinese medicine compounds, natural active products, small chemical molecules, biological agents and targeted anti-inflammatory drugs, serving as an essential core standard model for basic and translational psoriasis research in dermatology and immunology.