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Multivariate Modeling Platform for Recurrent Psoriasis: Recreating Lesional Pathological Features to Accelerate Dermatological Drug Validation

　　Psoriasis is a common dermatological condition characterized by erythematous plaques covered with silvery scales on the scalp, trunk, and extremities. It tends to recur and persist, significantly impacting patients’ physical and mental well-being. The pathogenesis of psoriasis is complex, resulting from the interplay of genetic factors, immune dysregulation, and environmental influences. Establishing an optimal animal model of psoriasis would greatly facilitate elucidation of its genetic basis, underlying mechanisms, and the development of novel therapeutics.

　　Common animal models of psoriasis

　　Psoriasis animal models can be classified into five categories: drug‑induced models, genetically engineered models, cytokine‑based models, xenograft models, and spontaneous mutation models.

　　| Drug-Induced Model

　　A drug‑induced model refers to a method in which topical application of a drug or feeding animals a diet deficient in essential fatty acids is used to elicit psoriasis‑like skin lesions and inflammatory responses. Currently, the most widely employed model is the imiquimod‑induced mouse model.

　　Case Study: Imiquimod-Induced Model by Aniphe BioLab:

　　| Laboratory Animals

　　6-week-old C57 male.

　　| Modeling Method

　　01. Shave a 2 cm × 3 cm area on the mouse’s back, then apply depilatory cream to the area to remove all hair completely.

　　02. Using a 1 mL syringe, draw up imiquimod ointment, expel any air from the syringe barrel, and inject 0.06 mL of the ointment into the depilated area, then spread it evenly.

　　03. After application, do not place the mice back into their cages immediately; allow 5–10 minutes for the cream to be partially absorbed before returning them.

　　04. Apply once daily for 5–10 consecutive days, and assess the skin weekly using the PASI score.

　　The scoring criteria are as follows:

　　Daily observation of the skin condition in the area treated with the medication; based on the PASI, the severity of back skin lesions (thickening, scaling, erythema) is scored on a scale from 0 to 4.

　　Based on the PASI, the severity of skin inflammation is assessed once daily, including measurements of skin erythema, scaling, and induration, with scores ranging from 0 to 4: 0 = none, 1 = mild, 2 = moderate, 3 = marked, and 4 = very marked.

　　| Experimental Evaluation System

　　① Skin lesion images:

　　

 

　　Image source: Aniphe BioLab

　　② HE results show:

　　

 

　　The results; image source: Aniphe BioLab.

　　Compared with the control group, the skin of mice treated with imq exhibited typical psoriasis‑like features, including acanthosis, inflammatory cell infiltration, and dermal vascular alterations.

　　| Model Features:

　　It is low-cost, highly operable, exhibits excellent reproducibility, requires a short modeling time, and produces skin lesions with a high degree of similarity.

　　| Other induction methods

　　① Cytokine model

　　Currently, injecting a series of cytokines—including IL‑23, IL‑12, IL‑36, IL‑22, and IL‑17C—into the skin of mice, in combination with Oncostatin‑M and IL‑33, has been employed to induce psoriasis‑like skin inflammation. Among the various cytokine‑injection mouse models, IL‑23 injection is the most commonly used approach; this cytokine has been administered in over 50 distinct genetically engineered mouse models to establish disease‑relevant phenotypes.

　　The cytokine‑induced psoriasis model is easy to establish, can be combined with various other genetically engineered mouse models, and does not require extensive time or resources for modeling; moreover, it is relatively inexpensive. However, the psoriasis‑like skin lesions induced by this model represent an acute inflammatory response that gradually resolves on their own once the injections are discontinued.

　　② Xenotransplantation model

　　Currently, the primary recipient strains for this type of model are nude mice, severe combined immunodeficiency (SCID) mice, and AGR129 mice. Among these, nude mice were the first to be used for such models; SCID mice are the most widely employed; and AGR129 mice are xenograft models in which functional T cells, B cells, and NK cells are absent due to the knockout of the RAG gene.

　　Because it requires obtaining substantial untreated lesional and non-lesional skin tissue as well as peripheral blood from psoriasis patients, and necessitates rapid tissue collection and transplantation to prevent graft ischemia and rejection, this model has not been widely adopted.

　　③ Spontaneous Mutation Model

　　Prominent examples of spontaneously mutant mouse models include the Asebia mouse, the scaly skin mouse (Fsn mouse), and the chronic proliferative dermatitis mouse. These spontaneous mutant mouse models all exhibit histopathological features characteristic of psoriasis; however, T cells and neutrophils are rarely observed in their histopathological sections, and they respond poorly to conventional therapies used for psoriasis.

　　As modeling techniques for psoriasis animal models have steadily advanced, the use of these spontaneous mutant mouse models has gradually faded from the scene, increasingly serving as the genetic background for other psoriasis animal models.

　　④ Genetic engineering model

　　Genetically engineered mouse models account for the largest proportion among all psoriasis mouse models; currently reported genetic mouse models of psoriasis primarily include transgenic mouse models and gene-knockout mouse models.

　　Gene-knockout mice can be further classified into complete and partial knockouts; by completely or partially knocking out specific genes in these mice, psoriasis‑like skin lesions can be induced.

　　Transgenic mouse models: These models are generated by using transgenic technology to overexpress specific genes in mice, thereby inducing psoriasis‑like skin lesions. Most such models achieve targeted gene overexpression by driving expression under the control of epidermal basal layer promoters, such as keratin 5 (K5), keratin 14 (K14), keratin 10 (K10), or involucrin, which in turn leads to the development of psoriasis‑like cutaneous manifestations.

　　Genetically engineered animal models, from a molecular and cellular perspective, manipulate specific single genes to induce psoriasis‑like skin pathology, thereby exhibiting high specificity. They enable the elucidation of the roles of particular genes in the pathogenesis of psoriasis and are well suited for examining the expression, function, and effects of individual genes. However, these models involve complex procedures, require substantial time, and are costly, and they cannot fully replicate the intricate processes underlying human psoriasis that arise from the combined actions of multiple genes. Consequently, there remains considerable room for further research in developing transgenic animal models of psoriasis.

　　Summary

　　It is believed that, as research into the pathogenesis of psoriasis deepens and more disease‑related genes are identified and characterized, an increasing number of animal models—more precise in reflecting the disease’s mechanisms and clinical features—will emerge, thereby providing more valuable insights for elucidating its pathogenic pathways and developing novel therapeutic strategies.

　　Aniphe BioLab offers a variety of approaches for establishing psoriasis animal models and provides pharmacological and efficacy evaluation services tailored to these disease models. We welcome inquiries from all clients!

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