RhoGTPases — NODes for effector-triggered immunity in animals

Stuart, Lynda M.; Boyer, Laurent

doi:10.1038/cr.2013.68

Cited by 8 publications

(9 citation statements)

References 10 publications

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“…In summary, recent evidence provides some support for the idea that the signaling pathways detecting diaminopimelic acid-type peptidoglycan in mammals and insects share a common ancestry (reviewed in [98]). This observation along with the finding that the Drosophila Toll protein and the homologous mammalian TLRs both function as cellular sensors of microbes highlights the conservation of innate immune surveillance mechanism within the animal kingdom.…”

Section: Evolution Of the Nod1 Signaling Pathwaymentioning

confidence: 96%

“…Interestingly, recent studies raise the possibility that the IMD and NOD1 signaling pathways represent evolutionary conserved signaling cascades for the detection of diaminopimelic acid-type peptidoglycan (reviewed in [98]). First, the E. coli CNF-1 toxin constitutively activates RAC2 in Drosophila cells, thereby inducing the IMD pathway [43] and diaminopimelic acid-type peptidoglycan activates the NOD1-signalling pathway in human cells through a RAC1-dependent mechanism [40].…”

Section: Evolution Of the Nod1 Signaling Pathwaymentioning

confidence: 99%

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Detection of enteric pathogens by the nodosome

Keestra

Bäumler

2014

Trends in Immunology

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Nucleotide-binding oligomerization domain protein (NOD)1 and NOD2 participate in signaling pathways that detect pathogen-induced processes, such as the presence of peptidoglycan fragments in the host cell cytosol, as danger signals. Recent work suggests that peptidoglycan fragments activate NOD1 indirectly, through activation of the small Rho GTPase Ras-related C3 botulinum toxin substrate 1 (RAC1). Excessive activation of small Rho GTPases by virulence factors of enteric pathogens also triggers the NOD1 signaling pathway. Many enteric pathogens use virulence factors that alter the activation state of small Rho GTPases, thereby manipulating the host cell cytoskeleton of intestinal epithelial cells to promote bacterial attachment or entry. These data suggest that the NOD1 signaling pathway in intestinal epithelial cells provides an important sentinel function for detecting ‘breaking and entering’ by enteric pathogens.

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Section: Evolution Of the Nod1 Signaling Pathwaymentioning

confidence: 96%

Section: Evolution Of the Nod1 Signaling Pathwaymentioning

confidence: 99%

Detection of enteric pathogens by the nodosome

Keestra

Bäumler

2014

Trends in Immunology

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“…22 Several studies indicate that the activation of Rho GTPases engages effective innate immune responses. 19 To address the relevance of ETI during infection, we chose the prototypic uropathogenic strain of E. coli UTI89 in which we deleted the HlyA gene to study the role of CNF1 without the interference of HlyA. We then established the kinetics of bacterial persistence in the blood.…”

Section: Host Responses To Effectortriggered Rho Gtpases Modificationmentioning

confidence: 99%

“…[13][14][15] A series of recent studies points to the capacity of host cells to perceive the activity of toxintargeting Rho GTPase, leading to inflammatory responses that are likely detrimental to the persistence of bacteria. [16][17][18][19] This system of recognition of the activity of toxins targeting Rho GTPase is related to Effector-Triggered Immunity (ETI). [19][20][21] Major innate immune signaling hubs comprising NOD and RIP proteins are essential in relaying Rho GTPase signaling to NF-kB.…”

Section: Introductionmentioning

confidence: 99%

“…[16][17][18][19] This system of recognition of the activity of toxins targeting Rho GTPase is related to Effector-Triggered Immunity (ETI). [19][20][21] Major innate immune signaling hubs comprising NOD and RIP proteins are essential in relaying Rho GTPase signaling to NF-kB. As discussed below, our recent data answer major questions raised by all these findings.…”

Section: Introductionmentioning

confidence: 99%

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Switching Rho GTPase activation into effective antibacterial defenses requires the caspase-1/IL-1beta signaling axis

Boyer

Lemichez²

2015

Small GTPases

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The pyrin inflammasome: from sensing RhoA GTPases-inhibiting toxins to triggering autoinflammatory syndromes

Jamilloux

Magnotti

Belot

et al. 2018

Pathogens and Disease

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Numerous pathogens including Clostridium difficile and Yersinia pestis have evolved toxins or effectors targeting GTPases from the RhoA subfamily (RhoA/B/C) to inhibit or hijack the host cytoskeleton dynamics. The resulting impairment of RhoA GTPases activity is sensed by the host via an innate immune complex termed the pyrin inflammasome in which caspase-1 is activated. The cascade leading to activation of the pyrin inflammasome has been recently uncovered. In this review, following a brief presentation of RhoA GTPases-modulating toxins, we present the pyrin inflammasome and its regulatory mechanisms. Furthermore, we discuss how some pathogens have developed strategies to escape detection by the pyrin inflammasome. Finally, we present five monogenic autoinflammatory diseases associated with pyrin inflammasome deregulation. The molecular insights provided by the study of these diseases and the corresponding mutations on pyrin inflammasome regulation and activation are presented.

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RhoGTPases — NODes for effector-triggered immunity in animals

Cited by 8 publications

References 10 publications

Detection of enteric pathogens by the nodosome

Detection of enteric pathogens by the nodosome

Switching Rho GTPase activation into effective antibacterial defenses requires the caspase-1/IL-1beta signaling axis

The pyrin inflammasome: from sensing RhoA GTPases-inhibiting toxins to triggering autoinflammatory syndromes

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