Regulation of inflammasome activation

By S. Man, T. Kanneganti. Immunological Reviews, 2015

966 citations recorded by the source corpus.

Inflammasome biology is one of the most exciting and rapidly growing areas in immunology. Over the past 10 years, inflammasomes have been recognized for their roles in the host defense against invading pathogens and in the development of cancer, auto‐inflammatory, metabolic, and neurodegenerative diseases. Assembly of an inflammasome complex requires cytosolic sensing of pathogen‐associated molecular patterns or danger‐associated molecular patterns by a nucleotide‐binding domain and leucine‐rich repeat receptor (NLR) or absent in melanoma 2 (AIM2)‐like receptors (ALR). NLRs and ALRs engage caspase‐1, in most cases requiring the adapter protein apoptosis‐associated speck‐like protein containing a CARD (ASC), to catalyze proteolytic cleavage of pro‐interleukin‐1β (pro‐IL‐1β) and pro‐IL‐18 and drive pyroptosis. Recent studies indicate that caspase‐8, caspase‐11, IL‐1R–associated kinases (IRAK), and receptor‐interacting protein (RIP) kinases contribute to inflammasome functions. In addition, post‐translational modifications, including ubiquitination, deubiquitination, phosphorylation, and degradation control almost every aspect of inflammasome activities. Genetic studies indicate that mutations in NLRP1, NLRP3, NLRC4, and AIM2 are linked with the development of auto‐inflammatory diseases, enterocolitis, and cancer. Overall, these findings transform our understanding of the basic biology and clinical relevance of inflammasomes. In this review, we provide an overview of the latest development of inflammasome research and discuss how inflammasome activities govern health and disease.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8d3f7d2615e1d785d28809d9ff84224841d9bdff

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In Molecular Biology

1. T. Kanneganti
2. Yuan He
3. G. Núñez
4. D. Sharma
5. H. Hara
6. Ting Liu
7. Lingyun Zhang
8. Donghyun Joo

Citations in the corpus

• Pseudomonas aeruginosa: pathogenesis, virulence factors, antibiotic resistance, interaction with host, technology advances and emerging therapeutics (2022, background): “Remarkably, TLRs are involved in the priming of inflammasome activation by promoting the transcription of inflammasomerelated genes.(290) NLRC4 and AIM2 (absent in melanoma 2) are well characterized among numerous inflammasome PRRs linked to infection of P.”
• Pyroptosis in inflammatory diseases and cancer (2022, background): “Extracellular LPS can induce the expression of type I interferon, which then forms a feedback loop and activates type I interferon receptor to induce caspase-11 expression [33, 34].”
• NF-κB signaling in inflammation (2017, positive): “60, 64 These diverse stimuli are thought to activate NLRP3 via inducing different cellular events, including K + efflux, Ca2 + signaling, mitochondrial and lysosomal damages that release substances such as reactive oxygen species, oxidized mitochondrial DNA and lysosomal proteases.”
• Mechanism and regulation of NLRP3 inflammasome activation (2016, background): “Emerging evidence indicates that several other members of the NLR family and the PYHIN family, including NLRP6, NLRP7, NLRP12, and IFI16, can also form inflammasomes, but their composition remains obscure [7].”
• The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “…include pathogen-derived ligands such as microbial cell wall components, nucleic acids, and pore-forming toxins; environmental crystalline pollutants like silica, asbestos, and alum; and endogenous danger signals like ATP, serum amyloid A, and uric acid crystals (Man and Kanneganti, 2015).”
• Pattern recognition receptors in health and diseases (2021, background): “The activated Caspase-1 spliced proIL-1β/proIL-18 into the corresponding mature cytokine.(193,296) There are five main types of inflammasomes that have been discovered, namely, NLRP1 inflammasome,(297) NLRP3 inflammasome,(298) NLRC4 inflammasome,(299,300) IPAF inflammasome, and AIM2 inflammasome.”