Cited by 244Inflammasome and immune disordersImmune Response and InflammationIL-33, ST2, and ILC Pathways

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Inflammasome Priming in Sterile Inflammatory Disease

Patel, Meghana N., Carroll, Richard G., Galván-Peña, Silvia, Mills, Evanna L., Olden, Robin, Triantafilou, Martha, Wolf, Amaya I., Bryant, Clare E., Triantafilou, Kathy, Masters, Seth L.·2017·Trends in Molecular Medicine

DOI 10.1016/j.molmed.2016.12.007

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Abstract

The inflammasome is a cytoplasmic protein complex that processes interleukins (IL)-1β and IL-18, and drives a form of cell death known as pyroptosis. Oligomerization of this complex is actually the second step of activation, and a priming step must occur first. This involves transcriptional upregulation of pro-IL-1β, inflammasome sensor NLRP3, or the non-canonical inflammasome sensor caspase-11. An additional aspect of priming is the post-translational modification of particular inflammasome constituents. Priming is typically accomplished in vitro using a microbial Toll-like receptor (TLR) ligand. However, it is now clear that inflammasomes are activated during the progression of sterile inflammatory diseases such as atherosclerosis, metabolic disease, and neuroinflammatory disorders. Therefore, it is time to consider the endogenous factors and mechanisms that may prime the inflammasome in these conditions.

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NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
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Authors: Patel, M. N., Carroll, R. G., Galván-Peña, S., Mills, E. L., Olden, R., Triantafilou, M., Wolf, A. I., Bryant, C. E., Triantafilou, K., & Masters, S. L.
Affiliations: GlaxoSmithKline (United Kingdom) (GB)
GlaxoSmithKline (United States) (US)
The University of Melbourne (AU)
Corresponding author: Masters, Seth L.
ORCID: Carroll, Richard G.
Galván-Peña, Silvia
Mills, Evanna L.
Triantafilou, Martha
Wolf, Amaya I.
Bryant, Clare E.
Triantafilou, Kathy
Masters, Seth L.
Venue: Trends in Molecular Medicine
Publisher: Elsevier BV
Published: 2017-02
Volume: 23
Issue: 2
Pages: 165-180
ISSN: 1471-4914 (ISSN-L)
DOI: 10.1016/j.molmed.2016.12.007
OpenAlex: W2572287198
Cited by: 241
References: 153
Citations by year: 2026: 12 · 2025: 17 · 2024: 15 · 2023: 24 · 2022: 29 · 2021: 25 · 2020: 37 · 2019: 31 · 2018: 33 · 2017: 17
FWCI: 3.02
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Molecular Medicine (publishedVersion)
PubMed (publishedVersion)
ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
Funders: Wellcome Trust
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Keywords: inflammasome priming, sterile inflammation, NLRP3 inflammasome, caspase-11, IL-1β processing, IL-18, pyroptosis, post-translational modification, atherosclerosis, metabolic disorders, neuroinflammation, Toll-like receptor ligands
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Alzheimer Disease, Animals, Humans, Immunity, Innate, Inflammation, Metabolic Diseases, Obesity, Neuroimmunomodulation, Atherosclerosis, Toll-Like Receptors, Interleukin-1beta, Hereditary Autoinflammatory Diseases, Inflammasomes

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Inflammasome Priming in Sterile Inflammatory Disease

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