TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD.

@article{Bikker2017TNFPI,
  title={TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD.},
  author={Rolf Bikker and Martin Christmann and Katharina Preu{\ss} and Bastian Welz and Judith Friesenhagen and Oliver Dittrich‐Breiholz and Ren{\'e} Huber and Korbinian Brand},
  journal={Cellular signalling},
  year={2017},
  volume={37},
  pages={
          123-135
        }
}
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16 Citations
Background Citations
6
Methods Citations
1
Results Citations
3

16 Citations

Citation Type

Citation Type

TNF Tolerance in Monocytes and Macrophages: Characteristics and Molecular Mechanisms
TLDR
It is concluded that TNF tolerance may represent a protective mechanism involved in the termination of inflammation and preventing excessive or prolonged inflammation and may also be a trigger of immune paralysis thus contributing to severe inflammatory diseases such as sepsis.
Activation of GSK3 Prevents Termination of TNF-Induced Signaling
TLDR
The data demonstrate that activation of GSK3 – either pathophysiologically or pharmacologically induced – may destroy the finely balanced condition necessary for the termination of inflammation-associated signaling.
GSK3: A Kinase Balancing Promotion and Resolution of Inflammation
TLDR
The role of GSK3 as a kinase balancing the initiation/perpetuation and the amelioration/resolution of inflammation is highlighted and its impact on pro-inflammatory cytokine/chemokine profiles, bacterial/viral infections, and the modulation of associated pro- inflammatory transcriptional and signaling pathways is discussed.
A20 Orchestrates Inflammatory Response in the Oral Mucosa through Restraining NF-κB Activity
TLDR
It is reported that A20 regulates inflammatory responses to a keystone oral bacterium, Porphyromonas gingivalis, and restrains periodontal inflammation through its effect on NF-κB signaling and cytokine production.
Proteome and Phosphoproteome Analysis in TNF Long Term-Exposed Primary Human Monocytes
TLDR
The experiments demonstrate that both proteome and phosphoproteome analysis can be effectively applied to study protein/phosphorylation patterns of primary monocytes and provide new regulatory candidates and evidence for a complex network of specific but synergistically acting/cooperating mechanisms enabling the affected cells to resist sustained TNF exposure and resulting in the resolution of inflammation.
Sepsis: From Historical Aspects to Novel Vistas. Pathogenic and Therapeutic Considerations.
TLDR
In this review, the description of pathogenic mechanisms of sepsis is propaedeutic to the illustration of novel therapeutic attempts for the prevention or attenuation of experimental sepsi as well as of clinical trials.
TNF‐&agr;–induced protein 3 (TNFAIP3)/A20 acts as a master switch in TNF‐&agr; blockade–driven IL‐17A expression
Vitamin E δ-tocotrienol inhibits TNF-α-stimulated NF-κB activation by up-regulation of anti-inflammatory A20 via modulation of sphingolipid including elevation of intracellular dihydroceramides.
The inhibitory effect of the deubiquitinase cylindromatosis (CYLD) on inflammatory responses in human gingival fibroblasts.
TLDR
The results suggest that CYLD participates in periodontal inflammatory responses by negatively regulating LPS-induced NF-κB signalling and knocking down CYLD expression greatly enhanced the mRNA expression of proinflammatory cytokines in L PS- or TNF-α-stimulated HGFs.
Decrease of miR-19b-3p in Brain Microvascular Endothelial Cells Attenuates Meningitic Escherichia coli-Induced Neuroinflammation via TNFAIP3-Mediated NF-κB Inhibition
TLDR
In vivo and in vitro findings indicate a novel quenching mechanism of the host by attenuating miR-19b-3p/TNFAIP3/NF-κB signaling in BMECs in response to meningitic E. coli, thus preventing CNS from further neuroinflammatory damage.
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