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Negative regulation of toll-like receptor-mediated signaling by Tollip.

http://www.ncbi.nlm.nih.gov/pubmed/11751856

Toll-like receptor (TLR)-mediated recognition of pathogens represents one of the most important mechanisms of innate immunity and disease resistance. The adaptor protein Tollip was identified initially as an intermediate in interleukin (IL)-1 signaling. Here we report that Tollip also associates directly with TLR2 and TLR4 and plays an inhibitory role in TLR-mediated cell activation. Inhibition by Tollip is mediated through its ability to potently suppress the activity of IL-1 receptor-associated kinase (IRAK) after TLR activation. In addition, we show for the first time that Tollip is a bona fide substrate for IRAK and is phosphorylated by IRAK upon stimulation with lipopolysaccharide or IL-1. Negative regulation of TLR signaling by Tollip may therefore serve to limit the production of proinflammatory mediators during inflammation and infection.

Pubmed ID: 11751856 RIS Download

Mesh terms: Carrier Proteins | Cell Line | Dose-Response Relationship, Drug | Drosophila Proteins | Escherichia coli | Humans | Immunoblotting | Interleukin-1 | Interleukin-1 Receptor-Associated Kinases | Intracellular Signaling Peptides and Proteins | Lipopolysaccharides | Membrane Glycoproteins | Phosphorylation | Plasmids | Precipitin Tests | Protein Binding | Protein Kinases | Protein Structure, Tertiary | Receptors, Cell Surface | Signal Transduction | Time Factors | Toll-Like Receptor 2 | Toll-Like Receptor 4 | Toll-Like Receptors

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Associated grants

  • Agency: NIAID NIH HHS, Id: R37 AI 33443
  • Agency: NIAID NIH HHS, Id: R37 AI033443

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