“Niu Pi Xian” we often hearis medically called “psoriasis”, which is a chronic recurrent disease, resulting in one or multiple red bumpy patches with silvery scales, and there is an apparent boundary between patches and normal skin. Psoriasis occurs at any age, incurring great individual and social burden. Then what are the design ideas for psoriasis? Let’s explore together.

We will share a paper entitled FXYD3 enhances IL-17A signaling to promote psoriasis by competitively binding TRAF3 in keratinocytes, published in Cellular and Molecular Immunology, with a high IF of 21.8. We hope to bring different inspirations.

1. Research background

(1) Despite undefined specific pathogenesis of psoriasis, the complex communication between keratinocytes and immune cells plays a critical role in disease initiation and maintenance.

(2) IL-23-IL-17 axis has been confirmed to be instrumental in psoriasis.

(3) IL-17-mediated NF-κB activation in keratinocytes plays an important role in psoriasis occurrence and maintenance.

(4) FXYD3 is mainly expressed in skin, colon, stomach and uterus, but its pathological effect and mechanism in skin diseases such as psoriasis awaits discovery.

2. Technical route

3. Research results

(1) FXYD3 expression is elevated in epidermis of psoriasis patients and IMQ mouse models

(2) FXYD3 ablation in keratinocytes attenuates psoriasis-like phenotypes in an IMQ mouse model

(3) FXYD3 ablation in keratinocytesre duces IMQ-induced psoriasis-like inflammation

(4) FXYD3 participates in psoriasis-likein flammation through IL-17-mediated signaling

(5) FXYD3 interacts with TRAF3

(6) FXYD3 targets TRAF3 to strengthen IL-17-mediated signaling

(7) FXYD3 competes with IL-17R and interacts with TRAF3

 4. Conclusion

The ultimate research results elucidate that FXYD3, as a mediator of IL-17 signaling in keratinocytes, forms a positive regulatory circuit to promote the exacerbation of psoriasis mechanism. Targeting FXYD3 may serve as a potential therapeutic method against psoriasis.