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. 2022 Nov 15;23(5):289–303. doi: 10.1038/s41577-022-00792-3

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Fig. 2 — a, Binding of tumour necrosis factor (TNF) to TNF receptor 1 (TNFR1) directly promotes inflammation by activating the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signalling pathways, which collectively lead to the transcriptional upregulation of genes encoding proinflammatory mediators, such as cytokines and chemokines. b, TNFR1 activation also indirectly promotes inflammation by triggering cell death. Lytic forms of cell death, such as apoptosis-driven secondary necrosis, pyroptosis and necroptosis, release damage-associated molecular patterns (DAMPs) that activate proinflammatory gene expression in bystander cells. In addition, the inflammatory response may originate from and/or be amplified by loss of barrier function caused by epithelial cell death (lytic and non-lytic) and the subsequent sensing of pathogen-associated molecular patterns (PAMPs) from microorganisms that have breached the epithelial barrier. PRR, pattern recognition receptor.