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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Immunol Rev. 2015 Mar;264(1):276–287. doi: 10.1111/imr.12273

Fig. 3. TNF excess triggers both host-beneficial and bacteria-beneficial molecular pathways.

Fig. 3

A schematic of chemical and genetic manipulations of TNF-induced pathways that mediate bacterial killing and macrophage necrosis. Abbreviations: TNFR, TNF receptor; RIP, receptor-interacting protein; MLKL, mixed lineage kinase-like; ROS, reactive oxygen species, CYPD, cyclophilin D; mPTPC, mitochondrial permeability transition pore complex; aSMase, acid sphingomyelinase.