期刊
FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.661162
关键词
pyroptosis; gasdermins; cell death; post-translational modifications; therapeutics; phosphorylation; inflammation
类别
资金
- Kennedy Trust, KTRR start-up fellowship [KENN 15 16 06]
- MRC New Investigator Grant [MR/S000623/1]
- Kennedy Trust, KTPS Studentship
- National University of Singapore Start Up grant
- Ministry of Education Inauguration Grant
Pyroptosis is a proinflammatory form of cell death mediated by gasdermin pores, releasing inflammatory cytokines. Gasdermin family members can also be cleaved by other proteases to form pores, contributing to various types of inflammation.
Pyroptosis is a proinflammatory form of cell death, mediated by membrane pore-forming proteins called gasdermins. Gasdermin pores allow the release of the pro-inflammatory cytokines IL-1 beta and IL-18 and cause cell swelling and cell lysis leading to release of other intracellular proteins that act as alarmins to perpetuate inflammation. The best characterized, gasdermin D, forms pores via its N-terminal domain, generated after the cleavage of full length gasdermin D by caspase-1 or -11 (caspase-4/5 in humans) typically upon sensing of intracellular pathogens. Thus, gasdermins were originally thought to largely contribute to pathogen-induced inflammation. We now know that gasdermin family members can also be cleaved by other proteases, such as caspase-3, caspase-8 and granzymes, and that they contribute to sterile inflammation as well as inflammation in autoinflammatory diseases or during cancer immunotherapy. Here we briefly review how and when gasdermin pores are formed, and then focus on emerging endogenous mechanisms and therapeutic approaches that could be used to control pore formation, pyroptosis and downstream inflammation.
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