In this issue, we introduce the Psoriasis Targeted Drug Evaluation Model—B6-hIL-17A Humanized Mice, which provides an improved platform for preclinical disease modeling of psoriasis treatments for effective and efficient clinical translation. First, let's uncover the pathology of psoriasis in order to better understand how the humanization of IL17A in mice can help researchers identify effective treatments.

What is Psoriasis?

Psoriasis is a chronic, recurring autoimmune skin disease that causes rapid generation of skin cells, which accumulate on the surface and lead to inflammation. Plaque Psoriasis, also known as “psoriasis vulgaris,” is the most common type which afflicts roughly 80% of all psoriasis patients. The main symptoms include a rash characterized by itchy, scaly patches appearing most commonly on areas such as the elbows, knees, lower back, and scalp. Approximately 125 million people worldwide suffer from psoriasis, accounting for 2% to 3% of the global population.[1] Psoriasis is associated with immune, genetic, environmental, and endocrine factors, which lead to abnormal proliferation and differentiation of skin cells, resulting in an excessive accumulation of skin cells on the skin’s surface. As both the mechanisms and treatments of psoriasis remain a hot topic in dermatological research, there is currently no cure. Patients primarily try to manage and control symptoms through a combination of identifying and avoiding triggers, topical treatments, phototherapy, systemic treatments, and lifestyle changes.


Figure 1. Schematic diagram of the differences between normal skin layers and psoriasis skin layers.[2]

Immune Dysregulation and Psoriasis

Research indicates that inflammation and autoimmunity play crucial roles in the onset and progression of psoriasis. The T cells of patients attack healthy skin cells and attract other immune cells, leading to inflammation and tissue damage within the skin. This results in the excessive proliferation and disordered differentiation of epidermal keratinocytes, causing new skin cells to be produced every few days and accumulate on the skin surface, developing the characteristic scaly, dry, raised skin patches known as plaques. The interleukin-23/interleukin-17 (IL-23/IL-17) pathway plays a central role in the autoimmune response in psoriasis, where IL-23 stimulates the production of the pro-inflammatory cytokine IL-17 by activating Th17 cells. In keratinocytes, IL-17A binds to its receptor, stimulating keratinocyte proliferation and leading to the release of inflammatory mediators and chemotactic factors, triggering an inflammatory response. Therefore, IL-17A is an important target for the treatment of inflammatory diseases, as demonstrated by monoclonal antibodies targeting IL-17A exhibiting therapeutic effects in patients with psoriasis.[3]

Figure 2. Impact of the IL-23/IL-17 pathway on epidermal keratinocytes in psoriatic skin.[4]

Cyagen has developed the
B6-hIL-17A humanized mouse model (Product Code: C001510) for research on targeted therapies against IL-17A. This model was successfully established as a psoriasis model using imiquimod (IMQ) induction and can be used to evaluate targeted drugs against human IL-17A.

Schematic Diagram of Model Construction and Drug Efficacy Evaluation

Application of imiquimod (IMQ) cream can induce skin damage and inflammation in mice that is similar to human psoriasis, making it a common induction method for preclinical research models. On the other hand, Ixekizumab is a humanized antibody that alleviates inflammation by binding to and neutralizing IL-17A, and is used to treat psoriasis and other autoimmune diseases.[5] The B6-hIL-17A humanized mouse model provides an improved platform for preclinical disease modeling of psoriasis treatments for effective and efficient clinical translation.

Figure 3. Establishment of the B6-hIL-17A mouse psoriasis model using IMQ induction and the experimental protocol for Ixekizumab efficacy validation.

Mouse Growth Curve

In both the treated and untreated groups subjected to IMQ, the weight change trends of the B6-hIL-17A mice and the wild-type mice are essentially consistent.

Figure 4. Growth curves of B6-hIL-17A mice and wild-type mice.

IMQ successfully induces a psoriasis-like phenotype in B6-hIL-17A mice

By the third day of consecutive application of IMQ ointment, the skin of B6-hIL-17A mice exhibited noticeable scaling and surface roughness, with some regions showing erythema, and the skin thickness slightly greater than normal - with scales in the most severe areas flaking off. After treatment with Ixekizumab, the skin condition of the B6-hIL-17A mice showed significant improvement.

Figure 5. Comparison of skin in 8-week-old wild-type mice, B6-hIL-17A mice, and B6-hIL-17A mice treated with Ixekizumab on the third day of IMQ induction.

IMQ induction leads to high expression of human IL-17A protein in B6-hIL-17A mice

IMQ induction triggers the activation and proliferation of immune cells in mice, resulting in increased expression of IL17A. ELISA results show that B6-hIL-17A mice induced with IMQ express >20 pg/mL of human IL-17A protein, while uninduced B6-hIL-17A do not exhibit detectable levels of human IL-17A protein (Figure 6). After treatment with Ixekizumab, the expression of human IL-17A protein in B6-hIL-17A mice is significantly reduced, bringing it to levels comparable to those in the control B6N and B6-hIL-17A mice.

Figure 6. ELISA results of human IL-17A protein expression in 8-week-old female B6-hIL-17A mice and wild-type mice.

Psoriasis Area and Severity Index (PASI)

According to the Psoriasis Area and Severity Index (PASI) scoring tool, we quantified the area and severity of skin lesions in various groups of mice. The results showed that after applying IMQ, the B6-hIL-17A mice developed symptoms such as skin lesions, scaling, erythema, and skin folds. Following treatment with Ixekizumab, the skin damage and inflammatory conditions in B6-hIL-17A mice were alleviated in a dose-dependent manner. In the high-dose Ixekizumab treatment group, the PASI scores were significantly lower compared to the untreated group.

Figure 7. PASI scores of 8-week-old B6-hIL-17A mice and wild-type mice after IMQ treatment and Ixekizumab therapy.

Ixekizumab effectively improves the histopathology of B6-hIL-17A mice

After applying IMQ, the skin of B6-hIL-17A mice exhibited psoriasis-like histopathological phenotypes, including hyperkeratosis or parakeratosis of the stratum corneum (outermost layer of skin), thinning or disappearance of the stratum granulosum (granular layer), thickening of the stratum spinosum (spinous layer), elongation or undulation of rete ridges, and infiltration of mononuclear or multinuclear cells in the dermis. Following treatment with Ixekizumab, these symptoms were significantly improved in the skin of B6-hIL-17A mice, with the therapeutic effects being dose-dependent.

Figure 8. H&E staining, histological scoring, and measurement of epidermal thickness in the skin of 8-week-old female B6-hIL-17A mice and wild-type mice controls.


Under normal conditions, the B6-hIL-17A mice can exhibit trace amounts of human IL-17A protein detectable through ELISA testing. Induction with imiquimod (IMQ) leads these mice to highly express human IL-17A protein, displaying psoriasis-like phenotypes such as skin roughness, scaling, erythema, and skin folds. Treatment with Ixekizumab can effectively inhibit the psoriasis-like histopathological phenotypes induced by IMQ in B6-hIL-17A mice and significantly reduce the levels of human IL-17A protein in their bodies, with therapeutic effects showing a dose-dependency. Therefore, the IMQ-induced B6-hIL-17A mouse model serves as an effective tool for studying the mechanisms of IL-17A related autoimmune diseases such as psoriasis and evaluating the efficacy of IL17A-targeted drugs.

In addition to our established models such as the B6-hIL-17A mouse model, Cyagen provides a variety of humanized models related to autoimmune and inflammatory diseases, including spontaneous and induced disease models. Contact us for a free consultation on your model customization project to see how we can enhance your preclinical research.


[1]National Psoriasis Foundation. (n.d.). Psoriasis statistics. Retrieved December 30, 2023, from
[2]DUOBRII. (n.d.). Psoriasis Facts. Retrieved December 30, 2023, from
[3]Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker JNWN. Psoriasis. Lancet. 2021 Apr 3;397(10281):1301-1315.
[4]Hawkes JE, Chan TC, Krueger JG. Psoriasis pathogenesis and the development of novel targeted immune therapies. J Allergy Clin Immunol. 2017 Sep;140(3):645-653.
[5]Craig S, Warren RB. Ixekizumab for the treatment of psoriasis: up-to-date. Expert Opin Biol Ther. 2020 Jun;20(6):549-557.