Fig. 8: Graphical abstract. | Nature Communications

Fig. 8: Graphical abstract.

From: Single cell transcriptomics of human psoriasis and epidermal specific Ube2l3 deficient mice highlight CXCL16/CXCR6 involvement in psoriasis development

Fig. 8

A psoriasis-like lesion mouse model was generated by conditional knock out Ube2l3 in epidermis (Ube2l3△Epi), which was compared with human psoriasis scRNA-seq data and facilitate cross-species comparisons of differentiation dynamics and ligand-receptor pathways in epidermis. In particular, IL-17A was regulated by CXCR6+ Vγ2+ γδT in mouse while CXCR6+ CD8+ T in human. Ube2l3 reduction in keratinocytes activated IL-1β and then promote CXCL16 expression through STAT3 signaling. CXCR6+γδT17/ Tc17cells are prevalent within the epidermal immune microenvironment of psoriasis. Neutralization of CXCL16 inhibits the progression of psoriasis-like lesions in Ube2l3△Epi mice. (Created in BioRender. Chen, X. (2025) https://BioRender.com/c9dlkqv).

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