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

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.

Purinergic keratinocyte-to-sensory neuron signaling is a ubiquitous amplification mechanism that is required for normal mechanical, cold, and heat sensation in vivo.

Optogenetics reveals that keratinocytes can evoke action potential firing in several types of cutaneous sensory afferents, including those that transmit thermal, mechanical and pain stimuli.

The adaptor proteins FADD and TRADD play an important role in the Sharpin-dependent anti-apoptosis signaling pathway in keratinocytes and regulate skin homeostasis.

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

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.

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

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

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.