Intrinsic defects in keratinocytes can cause skin inflammation through excessive cell death and production of inflammatory molecules.

An intracellular ion channel may have a central role in the release of cytokines by macrophages.

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.

Polarity cascade initiated by aPKC in the periderm is transduced by adherens junction component E-cadherin to the basal epidermis during the development of zebrafish bilayered epidermis.

The sequencing of microbial genomes reveals that the presence of a particular microbial species in the gut may increase the risk of the autoimmune disease rheumatoid arthritis.

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

Text mining of complete EHRs for 14,017 diabetes patients and subsequent clustering led to phenotypically deep clusters, showing distinct glycemic profiles, comorbidities, and SNP association patterns.

Direct and selective activation of TRPML2 promotes macrophage migration through release of CCL2.