Psoriasis

Psoriasis

Psoriasis is a chronic immune-mediated skin disorder characterized by erythematous plaques, scaling, and dysregulated keratinocyte proliferation. To address diverse therapeutic development needs, we offer two validated psoriasis models with distinct mechanistic profiles:

Model

IMQ-induced Psoriasis

Feature

TLR7/8 activation → IFN-α/IL-23 axis

Plasmacytoid DCs, Neutrophils, Th17

Mimics early-stage innate immune response

Model

hIL23-induced Psoriasis

Feature

Direct IL-23/Th17 axis activation

Tissue-resident γδ T cells, Th17

Recapitulates IL-23-driven pathogenesis

For more information:

hIL-23-induced Psoriasis​

hIL-23-induced Psoriasis​

The hIL-23 Injection Model utilizes the activation of the IL-23/Th17 signaling axis, inducing sustained keratinocyte proliferation and elevated IL-17A, IL-17F expression. This model mirrors human plaque psoriasis with enhanced vascular remodeling and tissue-resident T-cell infiltration, making it suitable for evaluating biologics targeting IL-23p19 or downstream JAK/STAT pathways.

The model strategy of hIL-23-induced psoriasis is shown in Fig.3A. Ear thickness increased after hIL-23 administration and was inhibited following infliximab treatment (Fig.3B). The weight of ear increased significantly after hIL-23 administration (Fig.3C). The inflammatory score of ear skin increased significantly as well as epidermal and dermal thickness (Figure. 3D&3E&3F). hIL-23 administration up-regulated the expression levels of mouse IL-17A, IL-17F, Defb4 and S100A7a in the ear skin (Fig.3G).

IMQ-induced Psoriasis

IMQ-induced Psoriasis

Imiquimod (IMQ)-induced psoriasis model replicates key human pathology through topical application of IMQ, activating the Th17/IL-23 signaling axis and inducing hallmark psoriatic features within 7 days.