Abstract
The inflammasome-forming NLRs are well characterized members of a protein complex mediating the activation of caspase-1 and the cleavage of pro-IL-1β and pro-IL-18 into their active, secreted forms. New data suggest that components of the inflammasome cascade may have roles in influencing inflammasome-independent pathways of cytokine production. These influences on other immune cytokine pathways are complemented by data suggesting that non-inflammasome cytokines can influence the activation of the inflammasome, either directly or by influencing transcription of inflammasome components. The crosstalk between these cytokine cascades may lead to increased abilities for the cell to respond to diverse pathogen threats.
Copyright © 2011 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / immunology
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Adaptor Proteins, Signal Transducing / metabolism
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Animals
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Caspase 1 / genetics
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Caspase 1 / immunology
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Caspase 1 / metabolism
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DEAD-box RNA Helicases / genetics
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DEAD-box RNA Helicases / immunology
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DEAD-box RNA Helicases / metabolism
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Gene Expression Regulation / immunology*
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Gene Regulatory Networks / immunology
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Humans
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Immunity, Innate*
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Inflammasomes / genetics
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Inflammasomes / immunology*
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Inflammasomes / metabolism
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Inflammation / genetics
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Inflammation / immunology*
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Inflammation / metabolism
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Interleukin-18 / genetics
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Interleukin-18 / immunology*
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Interleukin-18 / metabolism
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Interleukin-1beta / genetics
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Interleukin-1beta / immunology*
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Interleukin-1beta / metabolism
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Macrophages / immunology
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Macrophages / metabolism
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Mice
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NF-kappa B / genetics
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NF-kappa B / immunology*
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NF-kappa B / metabolism
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Signal Transduction / immunology*
Substances
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Adaptor Proteins, Signal Transducing
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Inflammasomes
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Interleukin-18
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Interleukin-1beta
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NF-kappa B
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Caspase 1
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DEAD-box RNA Helicases