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. Author manuscript; available in PMC: 2020 May 30.
Published in final edited form as: Annu Rev Immunol. 2020 Jan 31;38:455–485. doi: 10.1146/annurev-immunol-111319-023800

Table 2.

Types of cell death

Type Immune effectors Morphological features Molecular features Characteristics
Complement-induced necrosis Complement Cell swelling, plasma membrane rupture Cell membrane pores Inflammatory
Killer cell-induced programmed cell death Perforin/granzymes Cell shrinkage, membrane blebbing, chromatin condensation, nuclear fragmentation Caspase activation (granzyme B), mitochondrial ROS, loss of mi to Δψ, proteolytic cascade, global mRNA decay, MOMP, cytochrome C release, genomic DNA fragmentation Noninflammatory
Apoptosis Death receptors/effector caspases, granzyme B Cell shrinkage, membrane blebbing, chromatin condensation, nuclear fragmentation Caspase activation, mitochondrial ROS, loss of mito Δψ, proteolytic cascade, global mRNA decay, MOMP, cytochrome C release, genomic DNA fragmentation Noninflammatory
Microptosis Perforin/granulysin/granzymes Parasites undergo cell death that morphologically resembles mammalian cell apoptosis Generation of superoxide anion, disruption of antioxidant defenses, disruption of protein synthesis and central metabolism Inflammatory
Pyroptosis Inflammasome/inflammatory caspases/gasdermins Membrane bubbles, cell flattening Inflammatory caspase activation, gasdermin cleavage, cell membrane pore, release of inflammatory intracellular contents Inflammatory
Necroptosis Death receptors/MLKL Cell swelling, cell membrane rupture RIPK1/3, MLKL phosphorylation, membrane ion channel, release of cellular contents Inflammatory

Abbreviations: MLKL, mixed lineage kinase domain-like pseudokinase; MOMP, mitochondrial outer membrane permeabilization; ROS, reactive oxygen species.