Targeting the differentiation regulators and/or AMPs of keratinocytes, rather than targeting immune cells, may be an alternative approach for topical anti-psoriatic treatment, an area with high need for new drugs.

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

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

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.

Overexpression of TCF7L1 overrides oncogenic Ras-induced senescence, induces cell migration, and promotes growth of skin squamous cell carcinoma independently of its interaction with β-catenin.

A Na,K-ATPase beta subunit can suppress basal cell carcinogenesis either via its osmoregulatory function to avoid hypotonic stress, or by promoting epithelial polarity and adhesiveness of basal keratinocytes from the overlying outer layer.

Thymic stromal cells help to develop and shape the gamma delta T cell pool.

Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.

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.

T cell receptor signaling is regulated by newly polymerized F-actin foci at the immunological synapse.