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.

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

Immune checkpoint inhibition therapy for cancer paradoxically activates tuberculosis infection, and advanced human cell culture modelling demonstrates excess TNF-α section is the primary driver.

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

A common mechanism might regulate the communal death of cells in flies and mammals.

Embryo-derived TNF promotes CPLA_2α phosphorylation and arachidonic acid release from luminal epithelium to induce fibroblast activation and decidualization.

Tn5 transposase has direct tagmentation activity towards RNA/DNA hybrids, which is harnessed as a more convenient and faster RNA-seq library construction method and will benefit RNA and chromatin research.

Analysis of rats carrying the microglia gene and Alzheimer risk factor Trem2^R47H variant shows increased glutamatergic transmission via supraphysiological TNF-α brain concentrations, linking a microglia pathogenic variant to neuronal dysfunction.

Pathological TNF-α-producing B cells are involved in the pathological process of polycystic ovary syndrome, and metformin inhibits mTOR phosphorylation, affects metabolic reprogramming, and further inhibits TNF-α expression in pathological B cells.