| pubmed-article:18006661 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C0679924 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C1571885 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C2698884 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C0003315 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C0971363 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C1548286 | lld:lifeskim |
| pubmed-article:18006661 | lifeskim:mentions | umls-concept:C1571886 | lld:lifeskim |
| pubmed-article:18006661 | pubmed:issue | 47 | lld:pubmed |
| pubmed-article:18006661 | pubmed:dateCreated | 2007-11-28 | lld:pubmed |
| pubmed-article:18006661 | pubmed:abstractText | There is increasing evidence that innate and adaptive immune responses are intimately linked. This linkage is in part mediated through the recognition of conserved microbial products by Toll-like receptors (TLRs). Detection of microbial products by TLRs can result in induction of inflammatory cytokines and activation of professional antigen-presenting cells, thereby enhancing adaptive immune responses. Here, we show that human beta-defensin-3 (hBD-3), an innate antimicrobial peptide, can induce expression of the costimulatory molecules CD80, CD86, and CD40, on monocytes and myeloid dendritic cells in a TLR-dependent manner. Activation of monocytes by hBD-3 is mediated by interaction with TLRs 1 and 2, resulting in signaling that requires myeloid differentiating factor 88 and results in IL-1 receptor-associated kinase-1 phosphorylation. In studies with HEK cells engineered to express various TLRs, we show that activation of NF-kappaB by hBD-3 depends on the expression of both TLR1 and TLR2. Thus, human TLR signaling is not restricted to recognition of microbial patterns but also can be initiated by host-derived peptides such as hBD-3. | lld:pubmed |
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| pubmed-article:18006661 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18006661 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18006661 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18006661 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:18006661 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:LedermanMicha... | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:SiegScott FSF | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:HardingCliffo... | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:DrageMichael... | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:FengZhiminZ | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:WeinbergAaron... | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:FunderburgNic... | lld:pubmed |
| pubmed-article:18006661 | pubmed:author | pubmed-author:JadlowskyJuli... | lld:pubmed |
| pubmed-article:18006661 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18006661 | pubmed:day | 20 | lld:pubmed |
| pubmed-article:18006661 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:18006661 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18006661 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18006661 | pubmed:pagination | 18631-5 | lld:pubmed |
| pubmed-article:18006661 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:18006661 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:18006661 | pubmed:articleTitle | Human -defensin-3 activates professional antigen-presenting cells via Toll-like receptors 1 and 2. | lld:pubmed |
| pubmed-article:18006661 | pubmed:affiliation | Departments of Molecular Biology and Microbiology and Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. | lld:pubmed |
| pubmed-article:18006661 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18006661 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18006661 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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