Unresponsiveness of MyD88-deficient mice to endotoxin.
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Summary
It is demonstrated that MyD88 knockout mice lack the ability to respond to LPS as measured by shock response, B cell proliferative response, and secretion of cytokines by macrophages and embryonic fibroblasts, and the inability of MyD 88 knockout mice to induce LPS-dependent gene expression cannot be attributed to lack of the activation of MAP kinases and NF-kappaB.
- Type
- article
- Published
- 1999-07-01
- Cited by
- 2,356
- References
- 47
- Access
- Open access
- OpenAlex
- https://openalex.org/W1996120614
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:26273328
Keywords
Biology, Immunology, Virology
References
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Cited by
- Innate immunity: Lipoproteins take their Toll on the host
- Immune Cell Activation by Bacterial Cpg-DNA through Myeloid Differentiation Marker 88 and Tumor Necrosis Factor Receptor–Associated Factor (Traf)6
- Toll‐like receptors: molecular mechanisms of the mammalian immune response
- MAP kinases in the immune response.
- Role of Toll-Like Receptors in Changes in Gene Expression and NF-κB Activation in Mouse Hepatocytes Stimulated with Lipopolysaccharide
- Cell activation by Porphyromonas gingivalis lipid A molecule through Toll-like receptor 4- and myeloid differentiation factor 88-dependent signaling pathway.
- Making and breaking tolerance.
- Lipopolysaccharide Stimulates p38-dependent Induction of Antiviral Genes in Neutrophils Independently of Paracrine Factors*
- CD19 regulates innate immunity by the toll-like receptor RP105 signaling in B lymphocytes.
- The immunogenic peptide for Th1 development.
- A low molecular weight mimic of the Toll/IL-1 receptor/resistance domain inhibits IL-1 receptor-mediated responses
- Essential role of IRF-3 in lipopolysaccharide-induced interferon-beta gene expression and endotoxin shock.
- Interferon- : an overview of signals, mechanisms and functions
- HSP60 and CpG-DNA-oligonucleotides differentially regulate LPS-tolerance of hepatic Kupffer cells.
- Chronic pneumonia despite adaptive immune response to Mycobacterium bovis BCG in MyD88-deficient mice
- RIP Links TLR4 to Akt and Is Essential for Cell Survival in Response to LPS Stimulation
- Variegation of the Immune Response with Dendritic Cells and Pathogen Recognition Receptors1
- Cellular reprogramming by gram‐positive bacterial components: a review
- Identification of Card15/Nod2 mRNA in intestinal tissue of experimentally induced colitis in rats.
- CD44 Is a Negative Regulator of Acute Pulmonary Inflammation and Lipopolysaccharide-TLR Signaling in Mouse Macrophages1
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