Regulation of inflammasome signaling

By Vijay A. K. Rathinam, S. Vanaja, Katherine A. Fitzgerald. Nature Immunology, 2012

936 citations recorded by the source corpus.

Innate immune responses have the ability to both combat infectious microbes and drive pathological inflammation. Inflammasome complexes are a central component of these processes through their regulation of interleukin 1β (IL-1β), IL-18 and pyroptosis. Inflammasomes recognize microbial products or endogenous molecules released from damaged or dying cells both through direct binding of ligands and indirect mechanisms. The potential of the IL-1 family of cytokines to cause tissue damage and chronic inflammation emphasizes the importance of regulating inflammasomes. Many regulatory mechanisms have been identified that act as checkpoints for attenuating inflammasome signaling at multiple steps. Here we discuss the various regulatory mechanisms that have evolved to keep inflammasome signaling in check to maintain immunological balance.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/940df3f554ff532f1e9fb153e544ec33ed1020a8

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Citations in the corpus

TRIF Licenses Caspase-11-Dependent NLRP3 Inflammasome Activation by Gram-Negative Bacteria (2012, neutral): “Given the significant potential of IL-1 and related cytokines to cause detrimental inflammation, key regulatory checkpoints ensure that inflammasome-dependent production of these cytokines is tightly regulated (Rathinam et al., 2012).”
The cGAS-cGAMP-STING pathway of cytosolic DNA sensing and signaling. (2014, background): “The AIM2 protein detects cytosolic DNA in myeloid cells to activate the inflammasome pathway, which leads to pyroptosis and the maturation of inflammatory cytokines including interleukin-1b (IL-1b) and IL-18 (Rathinam et al., 2012).”
Unified Polymerization Mechanism for the Assembly of ASC-dependent Inflammasomes (2014, background): “…in NLR inflammasome activation have 1194 Cell 156, 1193–1206, March 13, 2014 ª2014 Elsevier Inc. been connected to psoriasis, type II diabetes, inflammatory bowel diseases, and Alzheimer’s disease (Franchi et al., 2012; Lamkanfi and Dixit, 2012; Rathinam et al., 2012; Strowig et al., 2012).”
Control of adaptive immunity by the innate immune system (2015, background): “When CD22 is engaged by its sialic acid ligand, it activates the lipid phosphatase SHIP, which converts phosphatidylinositol-(3,4,5)trisphosphate (generated by PI(3)K) into phosphatidylinositol-(3,4)-bisphosphate and thus inhibits downstream steps in the PI(3)K signaling pathway96.”
The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “…three triggers, oxidative stress, lysosomal destabilization, and P2X7 receptor activation, like in other cell types, may work in concert to activate the inflammasome in the RPE (Bartlett et al., 2013; Cruz et al., 2007; Rathinam et al., 2012; Schroder and Tschopp, 2010; Wang and Sluyter, 2013).”
Stress, Inflammation, and Defense of Homeostasis (2014, background): “The NLRP3 inflammasomes, on the other hand, monitor membrane integrity and can sense pore-forming toxins, crystals, and many other noxious stimuli (Rathinam et al., 2012).”
Role of pyroptosis in inflammation and cancer (2022, background): “Inflammasomes identified thus far include members of the NLR family (nucleotide binding and oligomerization domains (Nod) and leucine-rich repeat-containing protein (NLR)), the PYHIN family (Pyrin domains and HIN-containing domains) and AIM2 (absent in melanoma 2) [37, 45].”