Inflammasomes

de Zoete, M. R.; Palm, N. W.; Zhu, S.; Flavell, R. A.

doi:10.1101/cshperspect.a016287

Cited by 322 publications

(255 citation statements)

References 191 publications

(238 reference statements)

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“…Although the full-length forms of IL-1a and IL-33 are biologically active, IL-1b and IL-18 require proteolytic processing to generate the active forms, an event typically associated with extracellular release [reviewed in (6,60)]. The most extensively studied protease involved in this process is caspase-1.…”

Section: Cytokine Activation Mechanismsmentioning

confidence: 99%

“…Caspase-1 is activated upon recruitment to an inflammasome ( Fig. 3A) comprising multiple copies of the adaptor protein apoptosisassociated speck-like protein (ASC) and sensor proteins [reviewed in (60)]. The sensor proteins are involved in directly or indirectly detecting cellular stress and microbial infections and can be divided into three main groups ( (60).…”

Section: Cytokine Activation Mechanismsmentioning

confidence: 99%

“…3A) comprising multiple copies of the adaptor protein apoptosisassociated speck-like protein (ASC) and sensor proteins [reviewed in (60)]. The sensor proteins are involved in directly or indirectly detecting cellular stress and microbial infections and can be divided into three main groups ( (60). In addition to cleaving pro-IL-1b and pro-IL-18, caspase-1 and the related caspase-4, caspase-5, and caspase-11 also cleave gasdermin D (61-63), which, in turn, oligomerizes in the plasma membrane to form pores (64-69) through which mature IL-1b and IL-18 can be released (Fig.…”

Section: Cytokine Activation Mechanismsmentioning

confidence: 99%

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Interleukin-36 cytokines may overcome microbial immune evasion strategies that inhibit interleukin-1 family signaling

Jensen

2017

Sci. Signal.

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Pathogens deploy immune evasion strategies to successfully establish infections within their hosts. Naturally, the host responds by acquiring mechanisms to counter these strategies. There is increasing evidence that the three interleukin-36 (IL-36) cytokines, IL-36a, IL-36b and IL-36g, play important roles in host immunity. With a focus on the skin as a target for microbial and viral invasion, the current knowledge of IL-36 functions is reviewed. Furthermore, the hypothesis that the IL-36s have evolved to counteract virulence factors is presented using viruses as an example. The IL-36s are related to IL-1a, IL-1b, IL-18, and IL-33. Numerous viruses affecting the skin have developed immune evasion strategies that neutralize IL-1a, IL-1b, or IL-18 signaling or combinations of these pathways. Through small differences in activation mechanisms and receptor utilization, it is possible that IL-36 signaling may proceed unhindered in the presence of these viral inhibitors. Thus, one physiological function of the IL-36s may be to counteract microbial immune evasion.

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Section: Cytokine Activation Mechanismsmentioning

confidence: 99%

Section: Cytokine Activation Mechanismsmentioning

confidence: 99%

Section: Cytokine Activation Mechanismsmentioning

confidence: 99%

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Interleukin-36 cytokines may overcome microbial immune evasion strategies that inhibit interleukin-1 family signaling

Jensen

2017

Sci. Signal.

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“…Caspase-1 has been shown to activate IL-1β and IL-18 proinflammatory cytokine precursors [57] . It has long remained unknown how their matured species translocate across the plasma membrane.…”

Section: Discussionmentioning

confidence: 99%

“…Caspase-1 is a cysteine protease and the common denominator of some twenty NLR/ALR inflammasome complexes identified so far and that contribute to host defenses against infections [57] . Cleavage sites for caspase-1 are present on HCV E2, NS2 and NS3 (http://web.…”

Section: Caspase-1 Is Required For the Release Of Hcv Particles Via Imentioning

confidence: 99%

Assembly and release of infectious hepatitis C virus involving unusual organization of the secretory pathway

Triyatni

Berger

Saunier

2016

WJH

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Institutional review board statement: Approved the use of serum IgG of a patient cured from an HCV infection for in vitro studies (Hôpital and Institut Cochin, Paris).Institutional animal care and use committee statement: Not applicable.Conflict-of-interest statement: Saunier B, Triyatni M and Berger EA are co-inventors on NIH-owned patent #US 9052321 B2 on the HCV particle production system. Triyatni M et al . Unusual secretory pathway of hepatitis C virus in thin section transmission electron microscopy. These findings were compared with the JFH-1 strain/Huh-7.5 cell model. RESULTS:We found that CANX was necessary for the production of HCV particles by BHK-WNV cells. This process involved the recruitment of a subset of HCV proteins, detected by immunoglobulin of an HCV-cured patient, in a compartment of rearranged membranes bypassing the endoplasmic reticulum-Golgi intermediary compartment and surrounded by mitochondria. It also involved the maturation of N-linked glycans on HCV envelope proteins, which was required for assembly and/or secretion of HCV particles. The formation of this specialized compartment required RAB1; upon expression of HCV structural genes, this compartment developed large vesicles with viral particles. RAB1 and alpha-tubulin were required for the release of HCV particles. These cellular factors were also involved in the production of HCVcc in the JFH-1 strain/Huh-7.5 cell system, which involves HCV RNA replication. The secretion of HCV particles by BHK-WNV cells presents similarities with a pathway involving caspase-1; a caspase-1 inhibitor was found to suppress the production of HCV particles from a full-length genome. CONCLUSION:Prior activity of the WNV subgenomic replicon in BHK-21 cells promoted re-wiring of host factors for the assembly and release of infectious HCV in a caspase-1-dependent mechanism. Core tip: Our system for production of authentic infectious hepatitis C virus (HCV) in non-humanized, nonhepatic cells involves the rearrangement of inner cellular membranes triggered by the replication of flaviviruses. The present results suggest that this feature relies on the re-wiring of host factors that usually contribute to the secretion of glycoproteins to generate an unusual secretory pathway. This model offers a new way to study the properties of free HCV particles, i.e. , independently from lipoproteins.Triyatni M, Berger EA, Saunier B. Assembly and release of infectious hepatitis C virus involving unusual organization of the secretory pathway.

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Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways

Rivers-Auty

Brough

2015

Eur J Immunol

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Recently, murine caspase-11 and its human orthologues, caspase-4 and caspase-5, have been the subjects of intense research interest [1]. Currently there is a particular focus on the role these caspases play in directly sensing Gram-negative infections and in the induction of interleukin 1β (IL-1β) via a noncanonical NLR family, pyrin domain (PYD) containing 3 (NLRP3) pathway. This issue of the European Journal of Immunology features three papers by Baker et al., and, that, together, provide a significant step forward in our understanding

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Inflammasomes

Cited by 322 publications

References 191 publications

Interleukin-36 cytokines may overcome microbial immune evasion strategies that inhibit interleukin-1 family signaling

Interleukin-36 cytokines may overcome microbial immune evasion strategies that inhibit interleukin-1 family signaling

Assembly and release of infectious hepatitis C virus involving unusual organization of the secretory pathway

Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways

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