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.

The centromeres in Malassezia species, by breakage or inactivation, facilitate genome rearrangements that can result in varying karyotypes and contribute to the evolution of these species.

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.

Skin inflammation in Sharpin-deficient mice is primarily due to TNFR1-dependent apoptosis, but necroptosis appears to play a bigger role in inflammation of internal organs.

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

Stereotactic body radiotherapy combined with immunotherapy and chemotherapy in neoadjuvant setting exhibited a promising anti-tumor activity and an acceptable safety profile in triple-negative breast cancer patients.