The hypothesis is proposed that activation of innate immunity is the primary mechanism of phenoptosis (programmed death of an organism). In support of the hypothesis, we discuss (i) the data on active release of signaling molecules from the cell producing excessive inflammation; (ii) the data on contribution of mitochondrial production of reactive oxygen species to immune response.
Keywords: damage-associated molecular patterns (DAMPs); inflammasome; inflammation; mitochondrially-targeted antioxidants; pathogen-associated molecular patterns (PAMPs); phenoptosis; programmed death.