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• W2079132454 abstract "Toll-like receptors (TLRs) signal through two main pathways: a myeloid differentiation factor (MyD)88-dependent pathway that acts via nuclear factor κB (NF-κB) to induce proinflammatory cytokines such as tumour necrosis factor-α (TNF-α) and a MyD88-independent pathway that acts via type I interferons to increase the expression of interferon-inducible genes. Repeated signalling through TLR4 and a number of other TLRs has been reported to result in a reduction in the subsequent proinflammatory cytokine response, a phenomenon known as TLR tolerance. In this study we have shown that, whilst NF-κB activation and production of TNF-α and interleukin-12 by murine RAW264.7 and J774.2 cells in response to stimulation by TLR4, -5, -7 or -9, was reduced by prior stimulation with TLR4, -5, -7 or -9 ligands, the primary stimulation of TLR3, which does not use the MyD88 pathway, did not reduce the TNF-α or interleukin-12 responses to subsequent TLR stimulation. The response to TLR3 stimulation was not diminished by prior TLR ligand exposure. Furthermore, the production of interferon-β (IFN-β) following stimulation of TLR3 or -4, which is MyD88-independent, was increased by prior activation of TLR4, -5, -7 or -9. In contrast, TLR9 ligand-induced IFN-β production, which is MyD88-dependent, was tolerized by prior TLR stimulation. These results are consistent with differential regulation of MyD88-dependent and MyD88-independent cytokine production following serial activation of TLRs." @default.
• W2079132454 created "2016-06-24" @default.
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• W2079132454 date "2007-01-01" @default.
• W2079132454 modified "2023-10-16" @default.
• W2079132454 title "Toll-like receptor interactions: tolerance of MyD88-dependent cytokines but enhancement of MyD88-independent interferon-? production" @default.
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• W2079132454 doi "https://doi.org/10.1111/j.1365-2567.2006.02485.x" @default.
• W2079132454 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2265871" @default.
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