Neutrophils are essential for itch in a mouse model of atopic dermatitis, and promote the transition from acute to chronic itch via induction of CXCL10/CXCR3 signaling.

Neonatal-origin dermal Tγδ17 cells are required to maintain normal keratinocytes and prevent spontaneous atopic dermatitis.

A mouse model of atopic dermatitis provides mechanistic evidence for an association between allergic disease and skin cancer.

In keratinocytes, the BRAF and RAF1 proteins work independently to balance the activity of mitogenic and stress kinase cascades and uphold the mechanical and immunological barrier functions of the epidermis.

Neutrophils are the first immune cells that enter the skin and cause itch in atopic dermatitis.

TMEM79 targets frizzled receptor for degradation through inhibiting USP8 and is required for Xenopus embryogenesis.

Osteoarthritis pathogenesis is driven by IgE-mediated mast cell activation.

Expression of a psoriasis-associated CARD14^E138A mutant in keratinocytes induces TNF-dependent localised skin and systemic inflammation independently of the adaptive immune system.

Immunological analysis of wild-type and Crlf2^-/- mice reveals a role for the cytokine thymic stromal lymphopoietin on memory CD8⁺ T-cell responses to viral infection, findings with potential translational implications.

A protein interaction screen revealed desmosomes as a scaffold for the COP9 de-neddylating complex, to promote epidermal differentiation by governing the balance of Nedd8 and Ubiquitin modifications on Epidermal Growth Factor Receptor.