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

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

Digital NF-κB signaling achieves orthogonal control over the probability of activation (percentage of activated cells) and dynamic response heterogeneity in the population via the area and shape of the input profile.

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.

Autophagy is critical for the turnover of inflammatory signaling complexes containing RHIM-domain proteins.

Sustained TNF-α induction consolidates transcriptional memory for faster, stronger, and more sensitive subsequent induction in an active DNA demethylation-dependent manner for memory genes including CALCB, a therapeutic target for migraine.

Secretion of the inflammatory cytokine TNF requires a protein called iTAP/FrmD8, which controls the cell surface stability of the TNF shedding machinery, iRhom2 and TACE/ADAM17.

Polarizing susceptibilities to recurrent bladder infection are shaped by a duality in TNFɑ-mediated inflammation dynamics upon challenge infection that is dictated by the outcome of the initial infection.

The iRhom2 protein, a catalytically inactive relative of rhomboid proteases, controls inflammation and growth factor signalling by acting as an essential multifunctional regulatory subunit of the cell surface shedding protease TACE (ADAM17).