The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

By B. Davis, Haitao Wen, J. Ting. Annual Review of Immunology, 2011

1,622 citations recorded by the source corpus.

Inflammasome activation leads to caspase-1 activation, which causes the maturation cleavage of pro-IL-1β and pro-IL-18. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a5e25cd04a2c93d457dce72a71801e690f805098

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Citations in the corpus

Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome. (2015, positive): “The NLRP3 inflammasome is a cytosolic protein complex composed of NLRP3, ASC, and caspase-1, and assembled in response to both microbial infection and endogenous ‘‘danger signal’’ (Davis et al., 2011; Martinon et al., 2009).”
Critical role for calcium mobilization in activation of the NLRP3 inflammasome (2012, neutral): “Stauffer TP, Ahn S, Meyer T (1998) Receptor-induced transient reduction in plasma membrane PtdIns(4,5)P2 concentration monitored in living cells.”
Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. (2013, background): “As shown in Figure 2A, we found that pretreatment with DHA inhibited caspase-1 cleavage and IL-1b secretion triggered by all examined agonists, including MSU, Alum, R837, and ATP, similar to nigericin.”
The pore forming protein gasdermin D regulates interleukin-1 secretion from living macrophages (2017, neutral): “This loss of membrane integrity results in the release of cytosolic lactate dehydrogenase (LDH) into the extracellular space, and the staining of intracellular nucleic acids by the membrane impermeable dye propidium iodide (PI) (Davis et al., 2011; Latz et al., 2013).”
The adapter MAVS promotes NLRP3 mitochondrial localization and inflammasome activation (2013, neutral): “Nod-like receptors (NLRs) are a family of cytosolic proteins containing several prototypic domains, including C-terminal leucine-rich repeats (LRRs), a central nucleotide binding or oligomerization domain (NBD, NOD, or NACHT), and N-terminal pyrin domain (PYD) that detect ligands of microbial or end”
Staphylococcus aureus Leukocidin A/B (LukAB) Kills Human Monocytes via Host NLRP3 and ASC when Extracellular, but Not Intracellular (2015, neutral): “innate immune responses [27].”