Jennifer P. Fox

This study identifies CD38 as a regulator of interferon responses in juvenile dermatomyositis and suggests its inhibition as a potential therapeutic strategy.

This study shows that IL-17 targets different cell types in inflammatory skin diseases, with fibroblasts being key in hidradenitis suppurativa and both fibroblasts and keratinocytes in psoriasis.

The paper investigates how particulate matter exposure affects nasal epithelial cells in chronic rhinosinusitis (CRS) and controls, finding amplified inflammatory and barrier dysfunction responses in CRS cells.

singIST quantifies disease model similarity to human conditions at single-cell resolution using pathway and cell type-level measures, demonstrating its utility in atopic dermatitis models.

The paper shows that restoring keratinocyte homeostasis reduces skin inflammation by reversing gene programs and normalizing epidermal architecture in a murine model.

The paper identifies TWEAK-IL-13 signaling as a driver of paradoxical skin reactions following anti-TNF, IL-17, or IL-23 therapy.

This study identifies interferon-responsive dermal fibroblasts in Sweet's syndrome that promote neutrophil recruitment through chemokine expression and spatial positioning.