| pubmed-article:9808181 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9808181 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:9808181 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
| pubmed-article:9808181 | lifeskim:mentions | umls-concept:C0014264 | lld:lifeskim |
| pubmed-article:9808181 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:9808181 | lifeskim:mentions | umls-concept:C1819439 | lld:lifeskim |
| pubmed-article:9808181 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:9808181 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:9808181 | pubmed:dateCreated | 1998-12-15 | lld:pubmed |
| pubmed-article:9808181 | pubmed:abstractText | Endotoxin tolerance, the down-regulation of a subset of endotoxin-driven responses after an initial exposure to endotoxin, may provide protection from the uncontrolled immunological activation of acute endotoxic shock. Recent data suggest, however, that the inhibition of monocyte/macrophage function associated with endotoxin tolerance can lead to an inability to respond appropriately to secondary infections in survivors of endotoxic shock. IL-12 production by antigen-presenting cells is central to the orchestration of both innate and acquired cell-mediated immune responses to many pathogens. IL-12 has also been shown to play an important role in pathological responses to endotoxin. We therefore examined the regulation of IL-12 during endotoxin tolerance. Priming doses of lipopolysaccharide ablate the IL-12 productive capacity of primary human monocytes. This suppression of IL-12 production is primarily transcriptional. Unlike the down-regulation of TNF-alpha under such conditions, the mechanism of IL-12 suppression during endotoxin tolerance is not dependent upon IL-10 or transforming growth factor-beta, nor is IL-12 production rescued by IFN-gamma or granulocyte-macrophage colony-stimulating factor. Of note, human dendritic cells also undergo endotoxin tolerance, with potent down-regulation of IL-12 production. Endotoxin tolerance-related suppression of IL-12 production provides a likely mechanism for the anergy seen during the immunological paralysis which follows septic shock. | lld:pubmed |
| pubmed-article:9808181 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9808181 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9808181 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9808181 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9808181 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:9808181 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:WysockaMM | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:TrinchieriGG | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:ONOS ISI | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:NutmanTT | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:WahlLL | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:KarpC LCL | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:ArmantMM | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:CuomoPP | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:MarovichMM | lld:pubmed |
| pubmed-article:9808181 | pubmed:author | pubmed-author:FactorR ERE | lld:pubmed |
| pubmed-article:9808181 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9808181 | pubmed:volume | 28 | lld:pubmed |
| pubmed-article:9808181 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9808181 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9808181 | pubmed:pagination | 3128-36 | lld:pubmed |
| pubmed-article:9808181 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:meshHeading | pubmed-meshheading:9808181-... | lld:pubmed |
| pubmed-article:9808181 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9808181 | pubmed:articleTitle | Potent suppression of IL-12 production from monocytes and dendritic cells during endotoxin tolerance. | lld:pubmed |
| pubmed-article:9808181 | pubmed:affiliation | Department of Medicine, Johns Hopkins University, Baltimore, MD, USA. ckarp@welchlink.welch.jhu.edu | lld:pubmed |
| pubmed-article:9808181 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9808181 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:9808181 | lld:pubmed |
