Аннотация:The aim of this research was to find out which isoforms of protein kinase C (PKC) are involved in Neutrophil Extracellular Trap (NET) formation activated by various stimuli, such as calcium ionophore A23187, PMA, and chemoattractant fMLP. Also, the role played by various PKC isoforms in reactive oxygen species (ROS) production was investigated. Neutrophils were isolated from the blood of healthy donors or patients with X-linked chronic granulomatous disease (CGD). ROS production was determined by luminol-amplified chemiluminescence assay. The release of NETs was detected using fluorescence microscopy.Using the inhibitory analysis on the model of oxidative burst, we showed that A23187 activates equally conventional (cPKCβ), novel (nPKCδ), and atypical (aPKCξ) PKC isoforms, while PMA and fMLP induce only PKCβ and PKCδ isoforms. NETosis of healthy donor neutrophils induced by A23187 and PMA depended on PKCβ and PKCξ isoforms. Using neutrophils isolated from patients with CGD activated A23187, we have shown that inhibitor of conventional PKC isoforms suppressed NET formation. Therefore, some additional unknown targets of PKCβ apart from NADPH oxidase subunits are involved in A23187-induced netotic pathway.