| pubmed-article:16751389 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16751389 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:16751389 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:16751389 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:16751389 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:16751389 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:16751389 | pubmed:dateCreated | 2006-6-5 | lld:pubmed |
| pubmed-article:16751389 | pubmed:abstractText | IL-12p70 is a key cytokine for the induction of Th1 immune responses. IL-12p70 production in myeloid cells is thought to be strictly controlled by T cell help. In this work we demonstrate that primary human monocytes can produce IL-12p70 in the absence of T cell help. We show that human monocytes express TLR4 and TLR8 but lack TLR3 and TLR7 even after preincubation with type I IFN. Simultaneous stimulation of TLR4 and TLR8 induced IL-12p70 in primary human monocytes. IL-12p70 production in peripheral blood myeloid dendritic cells required combined stimulation of TLR7/8 ligands together with TLR4 or with TLR3 ligands. In the presence of T cell-derived IL-4, but not IFN-gamma, stimulation with TLR7/8 ligands was sufficient to stimulate IL-12p70 production. In monocytes, type I IFN was required but not sufficient to costimulate IL-12p70 induction by TLR8 ligation. Furthermore, TLR8 ligation inhibited LPS-induced IL-10 in monocytes, and LPS alone gained the ability to stimulate IL-12p70 in monocytes when the IL-10 receptor was blocked. Together, these results demonstrate that monocytes are licensed to synthesize IL-12p70 through type I IFN provided via the Toll/IL-1R domain-containing adaptor inducing IFN-beta pathway and the inhibition of IL-10, both provided by combined stimulation with TLR4 and TLR8 ligands, triggering a potent Th1 response before T cell help is established. | lld:pubmed |
| pubmed-article:16751389 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16751389 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16751389 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16751389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16751389 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16751389 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16751389 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:EndresStefanS | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:HartmannGunth... | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:HornungVeitV | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:GieseThomasT | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:GillesStefani... | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:AblasserAndre... | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:Bekeredjian-D... | lld:pubmed |
| pubmed-article:16751389 | pubmed:author | pubmed-author:RothSusanne... | lld:pubmed |
| pubmed-article:16751389 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16751389 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16751389 | pubmed:volume | 176 | lld:pubmed |
| pubmed-article:16751389 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16751389 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16751389 | pubmed:pagination | 7438-46 | lld:pubmed |
| pubmed-article:16751389 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:16751389 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16751389 | pubmed:articleTitle | T cell-independent, TLR-induced IL-12p70 production in primary human monocytes. | lld:pubmed |
| pubmed-article:16751389 | pubmed:affiliation | Department of Internal Medicine, Division of Clinical Pharmacology, University of Munich, Germany. | lld:pubmed |
| pubmed-article:16751389 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16751389 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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