Tollip Regulates Proinflammatory Responses to Interleukin-1 and Lipopolysaccharide
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Summary
Tollip controls the magnitude of inflammatory cytokine production in response to IL-1β and LPS, and the production of the proinflammatory cytokines, IL-6 and tumor necrosis factor alpha was significantly reduced after IL- 1β andLPS treatment at low doses but not at lethal doses of LPS.
- Type
- article
- Published
- 2006-02-01
- Cited by
- 208
- References
- 21
- Access
- Open access
- OpenAlex
- https://openalex.org/W2141691560
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:30198274
Keywords
Proinflammatory cytokine, TLR4, Biology, Lipopolysaccharide, Tumor necrosis factor alpha
References
- Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor
- Cooperation of Toll-Like Receptor 2 and 6 for Cellular Activation by Soluble Tuberculosis Factor and Borrelia burgdorferi Outer Surface Protein A Lipoprotein: Role of Toll-Interacting Protein and IL-1 Receptor Signaling Molecules in Toll-Like Receptor 2 Signaling1
- Human Intestinal Epithelial Cells Are Broadly Unresponsive to Toll-Like Receptor 2-Dependent Bacterial Ligands: Implications for Host-Microbial Interactions in the Gut 1
- Flagellin Promotes Myeloid Differentiation Factor 88-Dependent Development of Th2-Type Response1
- Toll-like receptor signalling
- The Interleukin-1 Receptor-associated Kinase Is Degraded by Proteasomes following Its Phosphorylation*
- Characterization of Tollip protein upon Lipopolysaccharide challenge.
- A ubiquitin‐binding motif required for intramolecular monoubiquitylation, the CUE domain
- Interactions of TOM1L1 with the Multivesicular Body Sorting Machinery*
- Tollip and Tom1 Form a Complex and Recruit Ubiquitin-conjugated Proteins onto Early Endosomes*
- Signal transduction and endocytosis: close encounters of many kinds
- Tom1, a VHS Domain-containing Protein, Interacts with Tollip, Ubiquitin, and Clathrin*
- Sequential Autophosphorylation Steps in the Interleukin-1 Receptor-associated Kinase-1 Regulate its Availability as an Adapter in Interleukin-1 Signaling*
- An advanced culture method for generating large quantities of highly pure dendritic cells from mouse bone marrow.
- Receptor-dependent mechanisms of cell stimulation by bacterial endotoxin.
- Mechanisms of cross hyporesponsiveness to Toll-like receptor bacterial ligands in intestinal epithelial cells.
- Inflammation suppressor genes: please switch out all the lights
- Negative Regulation of Toll-like Receptor-mediated Signaling by Tollip*
- Inhibition of Interleukin 1 Receptor/Toll-like Receptor Signaling through the Alternatively Spliced, Short Form of MyD88 Is Due to Its Failure to Recruit IRAK-4
- IRAK-M is a negative regulator of Toll-like receptor signaling.
Cited by
- Gamma irradiation enhanced Tollip‐mediated anti‐inflammatory action through structural modification of quercetin in lipopolysaccharide‐stimulated macrophages
- Macrophage proinflammatory activation and deactivation: a question of balance.
- NF-κB and the immune response
- A study of the modulation of Toll-like receptor signalling in macrophages by Annexin-1
- Probing the Mechanisms Underlying the Regulatory Effects of Cactin in Innate Immune Signalling Pathways
- The Ubiquitin-like modifier FAT10 in tolerance induction
- Polymorphisms in the TOLLIP Gene Influence Susceptibility to Cutaneous Leishmaniasis Caused by Leishmania guyanensis in the Amazonas State of Brazil
- Endocytic Adaptor Protein Tollip Inhibits Canonical Wnt Signaling
- Innate immunity in atopic dermatitis.
- Potent suppression of arginase 1 expression in murine macrophages by low dose endotoxin.
- The chemical and computational biology of inflammation
- Investigation of the expression and biological response of the IL-1Rrp2 receptor in human cells
- Differential Expression of Novel Tyrosine Kinase Substrates during Breast Cancer Development *S
- Immunogenomics and systems biology of vaccines
- IL‐33 causes selective mast cell tolerance to bacterial cell wall products by inducing IRAK1 degradation
- Toll‐interacting protein contributes to mortality following myocardial infarction through promoting inflammation and apoptosis
- Biochemical and functional study of the immunomodulatory capacity of the soluble form of human Toll-like receptor 2
- TLR4 Signaling Inhibitory Pathway Induced by Green Tea Polyphenol Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor
- Identification and characterization of innate immune receptor substrates of γ-secretase enzyme complex
- Reciprocal Expression and Signaling of TLR4 and TLR9 in the Pathogenesis and Treatment of Necrotizing Enterocolitis
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