Innate immune detection of the type III secretion apparatus through the NLRC4 inflammasome
By Edward A. Miao, Dat P. Mao, Natalya Yudkovsky, Richard Bonneau, C. Lorang, S. Warren, I. Leaf, Alan Aderem. Proceedings of the National Academy of Sciences of the United States of America, 2010
812 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5524f6c40d4ec2ae901fea0bccd9accbfde4ed70
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Citations in the corpus
- Inflammasomes and their roles in health and disease. (2012, background): “The critical role of inflammasome signaling in protection against colon inflammation was confirmed in mice lacking ASC and caspase-1 (Allen et al. 2010, Dupaul-Chicoine et al. 2010, Zaki et al. 2010a) as well as in animals lacking IL-1β and IL-18 or their cognate receptors (Lebeis et al. 2009, Salce”
- Role of pyroptosis in inflammation and cancer (2022, background): “The NLRC4 inflammasome has been studied in-depth in a mouse model, wherein it is shown that the expression of NLRC4 is typically induced by bacterial flagellin or PrgJ, both components of the bacterial type III secretion system (T3SS) apparatus [54].”
- Inflammasomes in neuroinflammatory and neurodegenerative diseases (2019, background): “…2006); NLRC4 detects intracellular flagellin and components of type III secretion systems (T3SS) of bacterial pathogens (Franchi et al, 2006; Miao et al, 2006, 2010); AIM2 physically binds cytosolic doublestranded DNA (dsDNA) (Hornung et al, 2009); and pyrin indirectly responds to toxins…”
- Differential requirement for Caspase-1 autoproteolysis in pathogen-induced cell death and cytokine processing (2010, background): “Nlrc4 appears to detect these pathogens by recognizing molecules, such as flagellin or the T3SS rod subunit, which are secreted into the host cell cytosol by bacteria (Lightfield et al., 2008; Miao et al., 2010).”
- Regulation of inflammasome activation (2015, background): “coli (EprJ and EscI), Shigella flexneri (MxiI), and Pseudomonas aeruginosa (PscI) (126).”
- Caspase functions in cell death and disease. (2013, background): “…Salmonella typhimurium, Burkholderia pseudomallei (BsaK), Escherichia coli (EprJ and EscI), Shigella flexneri (MxiI), Pseudomonas aeruginosa (PscI), and Legionella pneumophila (Amer et al. 2006; Franchi et al. 2006, 2007; Miao et al. 2006, 2008, 2010; Molofsky et al. 2006; Sutterwala et al. 2007).”
- Mechanisms and functions of inflammasomes. (2014, background): “…components of pathogenic bacteria: flagellin, the building block of their locomotion machinery, and proteins from the type III and IV bacterial secretion systems that inject virulence factors into the host cell (Amer et al., 2006; Franchi et al., 2006; Miao et al., 2006; Miao et al., 2010b).”
- The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases (2011, background): “Together, these data suggest that flagellin gains entry to the host cytosol via T3SS or T4SS.”
- Pyroptotic cell death defends against intracellular pathogens (2015, background): “typhimurium was engineered to express the SPI-1 T3SS rod protein, PrgJ during systemic infection (26).”
- Caspase-1 induced pyroptotic cell death (2011, background): “typhimurium strains that persistently express flagellin or an NLRC4 detected T3SS rod protein and found that in both cases the bacteria were rendered severely attenuated via NLRC4-dependent Caspase-1 activation (19, 59).”