Inflammatory caspases are innate immune receptors for intracellular LPS

By Jianjin Shi, Yue Zhao, Yupeng Wang, Wenqing Gao, Jingjin Ding, Peng Li, Liyan Hu, F. Shao. Nature, 2014

2,123 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/172a4ac09aae3f1d49e7e41635e4be529efa7b32

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Citations in the corpus

From pyroptosis, apoptosis and necroptosis to PANoptosis: A mechanistic compendium of programmed cell death pathways (2021, background): “In addition, pyroptosis can also be induced by murine CASP11 or human CASP4/5-mediated non-canonical inﬂammasome activation in response to intracellular lipopolysaccharide (LPS) sensing [65–67].”
Caspases in cell death, inflammation and disease (2019, background): “In this pathway, internalized lipopolysaccharide (LPS) from Gram-negative bacteria interacts with the CARD domain and activates human caspases 4 and 5 and murine caspase-11 (Baker et al., 2015; Hagar et al., 2013; Kayagaki et al., 2013; Schmid-Burgk et al., 2015; Shi et al., 2014).”
Caspases in Cell Death, Inflammation, and Gasdermin-Induced Pyroptosis (2020, background): “Wang J, Sahoo M, Lantier L,Warawa J, Cordero H, et al. 2018 Caspase-11-dependent pyroptosis of lung epithelial cells protects from melioidosis while caspase-1 mediates macrophage pyroptosis and production of IL-18.”
Regulation of inflammasome activation (2015, background): “Caspase-8-deficient dendritic cells release IL-1b following LPS stimulation independently of an NLRP3 activator (Signal 2), but instead, requires RIP1, RIP3, MLKL, and PGAM5 (67).”
Pyroptotic cell death defends against intracellular pathogens (2015, background): “A recent study, however, demonstrated that caspase-11 is itself the LPS sensor, upending the dogma of caspase activation (98).”
Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling (2014, background): “When high concentrations of LPS persist in the body, LPS can be aberrantly found in the cytoplasm of macrophages where it binds to murine caspase-11 (human caspase-4 and -5) and activates a noncanonical inflammasome leading to the generation of proinflammatory IL-1b and IL-11, and to pyroptosis [37–”
Pattern Recognition Receptors and the Host Cell Death Molecular Machinery (2018, background): “During intracellular gram-negative bacteria infections, Lipid A, a component of LPS, can directly bind to the CARD domain of pro-caspase-11 (143), which gets activated and induces pyroptosis.”
Mechanism and regulation of NLRP3 inflammasome activation (2016, background): “Surprisingly, LPS binds directly to the CARD domains of caspase-11, human caspase-4, and caspase-5, but not other caspases [65].”
Inflammation and atherosclerosis: signaling pathways and therapeutic intervention (2022, background): “The noncanonical NLRP3 activation pathway is initiated by these caspases direct binding to intracellular LPS (iLPS) produced by Gram-negative bacteria, independent of TLR4, the conventional LPS receptor.(162) For example, caspase-4, -5, and -11 can indirectly promote the mature pro-IL-1β and pro-IL-”
Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death. (2017, background): “The NLRP3 inflammasome is absent in many human nonmonocytic cells that harbor a functional caspase-4-mediated LPS sensing pathway [25].”
Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis (2015, background): “Caspase-11 is activated by cytosolic lipopolysaccharide (LPS) receptors via the CARD domain [20].”