|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0023810,
umls-concept:C0185117,
umls-concept:C1274040,
umls-concept:C1510506,
umls-concept:C1515021,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C1879547,
umls-concept:C2911684
|
|
pubmed:issue |
10
|
|
pubmed:dateCreated |
2001-11-7
|
|
pubmed:abstractText |
Bacterial lipopolysaccharide (LPS) triggers innate immune responses through Toll-like receptor (TLR) 4, a member of the TLR family that participates in pathogen recognition. TLRs recruit a cytoplasmic protein, MyD88, upon pathogen recognition, mediating its function for immune responses. Two major pathways for LPS have been suggested in recent studies, which are referred to as MyD88-dependent and -independent pathways. We report in this study the characterization of the MyD88-independent pathway via TLR4. MyD88-deficient cells failed to produce inflammatory cytokines in response to LPS, whereas they responded to LPS by activating IFN-regulatory factor 3 as well as inducing the genes containing IFN-stimulated regulatory elements such as IP-10. In contrast, a lipopeptide that activates TLR2 had no ability to activate IFN-regulatory factor 3. The MyD88-independent pathway was also activated in cells lacking both MyD88 and TNFR-associated factor 6. Thus, TLR4 signaling is composed of at least two distinct pathways, a MyD88-dependent pathway that is critical to the induction of inflammatory cytokines and a MyD88/TNFR-associated factor 6-independent pathway that regulates induction of IP-10.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-3,
http://linkedlifedata.com/resource/pubmed/chemical/Interferons,
http://linkedlifedata.com/resource/pubmed/chemical/Irf3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lipid A,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Myd88 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Myeloid Differentiation Factor 88,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/TNF Receptor-Associated Factor 6,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Nov
|
|
pubmed:issn |
0022-1767
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
15
|
|
pubmed:volume |
167
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
5887-94
|
|
pubmed:dateRevised |
2008-11-21
|
|
pubmed:meshHeading |
pubmed-meshheading:11698465-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:11698465-Animals,
pubmed-meshheading:11698465-Antigens, Differentiation,
pubmed-meshheading:11698465-Cells, Cultured,
pubmed-meshheading:11698465-Chemokine CXCL10,
pubmed-meshheading:11698465-Chemokines, CXC,
pubmed-meshheading:11698465-DNA-Binding Proteins,
pubmed-meshheading:11698465-Drosophila Proteins,
pubmed-meshheading:11698465-Gene Deletion,
pubmed-meshheading:11698465-Interferon Regulatory Factor-3,
pubmed-meshheading:11698465-Interferons,
pubmed-meshheading:11698465-Lipid A,
pubmed-meshheading:11698465-Macrophages,
pubmed-meshheading:11698465-Membrane Glycoproteins,
pubmed-meshheading:11698465-Mice,
pubmed-meshheading:11698465-Models, Biological,
pubmed-meshheading:11698465-Myeloid Differentiation Factor 88,
pubmed-meshheading:11698465-NF-kappa B,
pubmed-meshheading:11698465-Proteins,
pubmed-meshheading:11698465-RNA, Messenger,
pubmed-meshheading:11698465-Receptors, Cell Surface,
pubmed-meshheading:11698465-Receptors, Immunologic,
pubmed-meshheading:11698465-Response Elements,
pubmed-meshheading:11698465-Signal Transduction,
pubmed-meshheading:11698465-TNF Receptor-Associated Factor 6,
pubmed-meshheading:11698465-Toll-Like Receptor 2,
pubmed-meshheading:11698465-Toll-Like Receptor 4,
pubmed-meshheading:11698465-Toll-Like Receptors,
pubmed-meshheading:11698465-Transcription Factors,
pubmed-meshheading:11698465-Transcriptional Activation
|
|
pubmed:year |
2001
|
|
pubmed:articleTitle |
Lipopolysaccharide stimulates the MyD88-independent pathway and results in activation of IFN-regulatory factor 3 and the expression of a subset of lipopolysaccharide-inducible genes.
|
|
pubmed:affiliation |
Department of Host Defense, Research Institute for Microbial Diseases, Japan Science and Technology Corporation, Osaka University, Osaka, Japan.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
