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.

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.

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

Excessive inflammation of the brain in early life predisposes individuals to neurodevelopmental disorders by preventing synapses from developing correctly.

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

A combination of transcriptomics, proteomics and modelling identifies a network of interacting protein phosphatases that act as a biological switch to move cells from the stem cell compartment to the differentiated compartment in cultured human epidermis.

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