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. 2023 Jan 10;13:1098725. doi: 10.3389/fimmu.2022.1098725

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Copyright © 2023 Zhang, Zhao, Zhou, Meng and Zhou

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Classic mechanisms of inflammasome activation. Lipopolysaccharide (LPS), which is regarded as the prototype of pathogen associated molecular patterns (PAMPs) and heat shock proteins (HSPs) as a typical representative of damage associated molecular patterns (DAMPs), can be recognized by toll-like receptor 4 (TLR4). Nuclear factor kappa B (NFκB) mediates these signals to produce NOD-like receptor family pyrin domain containing 3 (NLRP3), pro-IL-1β, pro-IL-18, and pro-IL-37. Next, NLRP3 is activated by potassium (K+) efflux, calcium (Ca2+) influx, and lysosomal leakage to recruit cysteine-requiring aspartate protease-1 (caspase-1). Caspase-1 then induces the maturation and release of pro-IL-1β, pro-IL-18, and pro-IL-37 and other related inflammatory agents that cause the inflammatory reaction and participate in the occurrence and development of the disease.