Molecular mechanisms involved in inflammasome activation

Germline-encoded pattern recognition receptors (PRRs) sense microbial or endogenous products released from damaged or dying cells and trigger innate immunity. In most cases, sensing of these signals is coupled to signal transduction pathways that lead to transcription of immune response genes that c...

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Vydané v:Trends in cell biology Ročník 19; číslo 9; s. 455 - 464
Hlavní autori: Bryant, Clare, Fitzgerald, Katherine A.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England Elsevier Ltd 01.09.2009
Predmet:
Adaptor Proteins, Signal Transducing - metabolism
Animals
Apoptosis Regulatory Proteins - metabolism
Caspase 1 - metabolism
Humans
Inflammation - genetics
Inflammation - immunology
Inflammation - metabolism
Pathology
Receptors, G-Protein-Coupled - immunology
Receptors, G-Protein-Coupled - metabolism
Signal Transduction
ISSN:0962-8924, 1879-3088, 1879-3088
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Popis
Shrnutí:Germline-encoded pattern recognition receptors (PRRs) sense microbial or endogenous products released from damaged or dying cells and trigger innate immunity. In most cases, sensing of these signals is coupled to signal transduction pathways that lead to transcription of immune response genes that combat infection or lead to cell death. Members of the NOD-like receptor (NLR) family assemble into large multiprotein complexes, termed inflammasomes. Inflammasomes do not regulate transcription of immune response genes, but activate caspase-1, a proteolytic enzyme that cleaves and activates the secreted cytokines interleukin-1β and interleukin-18. Inflammasomes also regulate pyroptosis, a caspase-1-dependent form of cell death that is highly inflammatory. Here, we review exciting recent developments on the role of inflammasome complexes in host defense and the discovery of a new DNA sensing inflammasome, and describe important progress made in our understanding of how inflammasomes are activated. Additionally, we highlight how dysregulation of inflammasomes contributes to human disease.
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ISSN:0962-8924
1879-3088
1879-3088
DOI:10.1016/j.tcb.2009.06.002