| pubmed-article:11698465 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C1510506 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C1515021 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:11698465 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:11698465 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:11698465 | pubmed:dateCreated | 2001-11-7 | lld:pubmed |
| pubmed-article:11698465 | 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. | lld:pubmed |
| pubmed-article:11698465 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11698465 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:11698465 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11698465 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11698465 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:KawaiTT | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:SatoSS | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:FujitaTT | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:HoshinoKK | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:InoueJJ | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:TakeuchiOO | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:MühlradtP FPF | lld:pubmed |
| pubmed-article:11698465 | pubmed:author | pubmed-author:AkiraSS | lld:pubmed |
| pubmed-article:11698465 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11698465 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11698465 | pubmed:volume | 167 | lld:pubmed |
| pubmed-article:11698465 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11698465 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11698465 | pubmed:pagination | 5887-94 | lld:pubmed |
| pubmed-article:11698465 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11698465 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11698465 | 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. | lld:pubmed |
| pubmed-article:11698465 | pubmed:affiliation | Department of Host Defense, Research Institute for Microbial Diseases, Japan Science and Technology Corporation, Osaka University, Osaka, Japan. | lld:pubmed |
| pubmed-article:11698465 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11698465 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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