Figure 1 NETosis pathways and potential therapeutic targets

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Figure 1 NETosis pathways and potential therapeutic targets Figure 1 | NETosis pathways and potential therapeutic targets. Stimulation of neutrophil receptors by microorganisms or sterile stimuli leads to release of calcium (Ca+) from the endoplasmic reticulum (ER), which results in activation of protein kinase C (PKC) and assembly of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex and/or mitochondrial activation, leading to generation of reactive oxygen species (ROS). Other cellular sources might also be important contributors of ROS. This ROS generation is followed by myeloperoxidase (MPO)-dependent migration of granular neutrophil elastase (NE) to the nucleus where it cleaves histones. In addition, peptidylarginine deiminase (PAD) 4 is activated and induces histone citrullination, which contributes to chromatin decondensation. Finally, the nuclear membrane is degraded and a mixture of chromatin and granular proteins is extruded from the cell. Extracellular DNase eventually degrades neutrophil extracellular traps (NETs). Modulation of critical steps in NET formation and degradation (shown by blocking arrows) might be beneficial for the treatment of autoimmune disorders. C5aR, C5a receptor; G-CSF: granulocyte colony stimulating factor; G-CSF-R, G-CSF receptor; FcγR, Fc γ receptor; TLR, Toll-like receptor. Gupta, S. & Kaplan, M. J. (2016) The role of neutrophils and NETosis in autoimmune and renal diseases Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.71