# FGF7 as an essential mediator for the onset of ankylosing enthesitis related to psoriatic dermatitis

## TL;DR

This study shows that FGF7 is crucial for joint inflammation in psoriatic arthritis, which is triggered by skin-related IL-17A.

## Contribution

The study identifies FGF7 as a key mediator linking skin and joint inflammation in psoriatic arthritis.

## Key findings

- IL-17A induces endochondral ossification via FGF7 signaling in mouse entheseal cultures.
- Blocking FGF receptor 2IIIb suppresses ankylosing enthesitis in a PsA animal model.
- FGF7 signaling plays a non-redundant role in joint pathology but not skin inflammation in PsA.

## Abstract

This study sheds light on the pathogenic association between the skin and joints in psoriatic arthritis. The authors indicated that IL-17A, which is produced in the skin, induces joint manifestations via FGF7 signaling in the pathology of psoriatic arthritis.

IL-17A plays an important role in the pathology of psoriasis and psoriatic arthritis (PsA). However, the pathogenic association between the skin and joint manifestations in PsA is not completely understood. In this study, we initially observed that IL-17A and FGF7 induced endochondral ossification in the mouse entheseal histoculture. Importantly, the responses of endochondral ossification by IL-17A stimulation were strongly inhibited by the treatment of a blocking antibody to FGF receptor 2IIIb, which is the receptor of FGF7, suggesting that FGF7 acts as a downstream factor of IL-17A in the endochondral ossification in the culture. Next, using the animal PsA model, the administration of an anti-FGF receptor 2IIIb antibody resulted in significant suppression of ankylosing enthesitis but not dermatitis. Collectively, our findings indicate that augmented IL-17A in PsA dermatitis induces the elevation of FGF7 levels in joint enthesis and results in a non-redundant role of FGF7 signaling in the development of ankylosing enthesitis in PsA.