Activation of Toll-like receptor (TLR), TNF receptor, or IL-1 receptor as well as phagocytosis of particles activates phagosomal NOX enzymes that leads to the production of reactive oxygen species (ROS). ROS inhibits caspase-1 by mediating the covalent modification of redox-sensitive cysteine residues. In the absence of NOX enzymes, ROS production is diminished and inhibition of caspase-1 is relieved, leading to enhanced IL-1β processing. Professional illustration by Debra T. Dartez.

Activation of Toll-like receptor (TLR), TNF receptor, or IL-1 receptor as well as phagocytosis of particles activates phagosomal NOX enzymes that leads to the production of reactive oxygen species (ROS). ROS inhibits caspase-1 by mediating the covalent modification of redox-sensitive cysteine residues. In the absence of NOX enzymes, ROS production is diminished and inhibition of caspase-1 is relieved, leading to enhanced IL-1β processing. Professional illustration by Debra T. Dartez.

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