Psoriasis
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- Autoimmune Diseases
- 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
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
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.
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