Abstract
Pyroptosis, caspase-1-dependent inflammatory cell death, is induced by intracellular pathogens or tissue lesions. Pro-caspase-1 activation, which is essential for the processing of proinflammatory cytokines pro-IL-1β and pro-IL-18, occurs in macromolecular protein complexes, also referred to as inflammasomes. In the gram-negative bacilli-induced infections inflammasome assembly incorporates caspase-4 and caspase-5. Originally identified as a protective mechanism of innate immunity, at present pyroptosis is not limited to the inhibition of intracellular pathogen multiplication. The current review discusses molecular mechanisms of pyroptosis-like cell death and possible pyroptosis involvement in tumor cell death.
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