The advances in pyroptosis initiated by inflammasome in inflammatory and immune diseases

Pyroptosis is a programmed and inflammatory cell death initiated by inflammasome. During pyroptosis, cytosolic pattern recognition receptors, apoptosis-associated speck-like protein and pro-Caspase-1 form activated inflammasome together. Caspase-1 activated by inflammasome results in generating an N-terminal cleavage product of gasdermin D (GSDMD), which is a major executor of pyroptosis. As a consequence of pyroptosis, a large number of pro-inflammatory cytokines are released including IL-1 beta and IL-18. Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and absent in melanoma 2 (AIM2)-like receptors (ALRs) belong to cytosolic pattern recognition receptors and assemble inflammasomes by detecting host cell damage signals. Pyroptosis pathways are divided into canonical and non-canonical pathways according to the identification of damage signals by cytoplasmic protein sensors. Pyroptosis not only plays an important role in infection, but also plays a vital role in inflammatory immune diseases. This article reviews the advances research of pyroptosis initiated by inflammasome in inflammatory and immune diseases.