Control of infection by pyroptosis and autophagy: role of TLR and NLR

@article{Bortoluci2010ControlOI,
  title={Control of infection by pyroptosis and autophagy: role of TLR and NLR},
  author={Karina Ramalho Bortoluci and Ruslan Medzhitov},
  journal={Cellular and Molecular Life Sciences},
  year={2010},
  volume={67},
  pages={1643-1651}
}
Cells can die by distinct mechanisms with particular impacts on the immune response. In addition to apoptosis and necrosis, recent studies lead to characterization of a new pro-inflammatory form of cell death, pyroptosis. TLR and NLR, central innate immune sensors, can control infections by modulating host cell survival. In addition, TLRs can promote the induction of autophagy, thus promoting delivery of infecting pathogens to the lysosomes. On the other hand, activation of some NLR members… 

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References

SHOWING 1-10 OF 64 REFERENCES

Pyroptosis: host cell death and inflammation

Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections.

Toll‐like receptor signaling in the lysosomal pathways

Recent views on how Toll‐like receptors direct microbes to final destruction by regulating the different pathways that lead to the lysosome are discussed.

NLRs at the intersection of cell death and immunity

Recent evidence demonstrating that NLR (nucleotide-binding domain, leucine-rich repeat containing) family proteins serve as a common component of both caspase-1-activated apoptotic pathways and caspases-independent necrotic pathways is reviewed.

Differential Regulation of Caspase-1 Activation, Pyroptosis, and Autophagy via Ipaf and ASC in Shigella-Infected Macrophages

Caspase-1 activation and IL-1β processing induced by Shigella are mediated through Ipaf, a cytosolic pattern-recognition receptor of the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family, and the adaptor protein apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC).

The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis

Members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC are critical components of the inflammasome that link microbial and endogenous 'danger' signals to caspase-1 activation.

MyD88 and Trif Target Beclin 1 to Trigger Autophagy in Macrophages*

It is demonstrated that not only TLR4, but also other TLR family members induce autophagy in macrophages, which is inhibited by MyD88, Trif, or Beclin 1 shRNA expression.

Fungal Zymosan and Mannan Activate the Cryopyrin Inflammasome*

It is shown that stimulation of macrophages and dendritic cells with heat-killed Saccharomyces cerevisiae or the purified cell wall components zymosan and mannan induced caspase-1 activation and IL-1β secretion when combined with ATP and suggested an important role for the Cryopyrin inflammasome during fungal infections.

Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome

A key role is shown for IPAF and capase-1 in innate immune responses to the pathogen P. aeruginosa, and it is demonstrated that virulent ExoU-expressing strains of P. Aerug inosa can circumvent this innate immune response.

Cutting Edge: Candida albicans Hyphae Formation Triggers Activation of the Nlrp3 Inflammasome1

It is shown that infection with Candida albicans is sensed by the Nlrp3 inflammasome, resulting in the subsequent release of IL-1β, which is consistent with a key role for NLRp3 in innate immune responses to the pathogen C.Albicans.

Toll‐like receptors control autophagy

It is shown that autophagy is controlled by recognizing conserved pathogen‐associated molecular patterns (PAMPs) and that the newly recognized ability of TLR ligands to stimulate Autophagy can be used to treat intracellular pathogens.
...