| pubmed-article:16365418 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16365418 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:16365418 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:16365418 | lifeskim:mentions | umls-concept:C1819479 | lld:lifeskim |
| pubmed-article:16365418 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:16365418 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16365418 | pubmed:dateCreated | 2005-12-20 | lld:pubmed |
| pubmed-article:16365418 | pubmed:abstractText | IL-12 drives type I immune responses and can mediate chronic inflammation that leads to host defense as well as disease. Recently, we discovered a novel role for 12/15-lipoxygenase (12/15-LO) in mediating IL-12p40 expression in atherosclerotic plaque and in isolated macrophages. We now demonstrate that 12/15-LO regulates IL-12 family cytokine production in a cell-type and stimulus-restricted fashion. LPS-stimulated elicited peritoneal macrophages derived from 12/15-LO-deficient (Alox15) mice produced reduced IL-12 and IL-23 levels, but comparable amounts of several other inflammatory mediators tested. Furthermore, LPS stimulation triggered an increase in wild-type macrophage 12/15-LO activity, whereas pharmacological inhibition of 12/15-LO activity suppressed LPS-induced IL-12 production in wild-type macrophages. 12/15-LO-deficient macrophages also produced reduced levels of IL-12 in response to TLR2 stimulation, but not in response to CpG (TLR9) or CD40/CD40L-mediated activation. In contrast to our previous finding of reduced IL-12 production in the setting of atherosclerosis, we found that comparable IL-12 levels were produced in Alox15 and wild-type mice during an acute response to LPS in vivo. This paradox may be explained by normal production of IL-12 by 12/15-LO-deficient neutrophils and dendritic cells, which are major sources of IL-12 during acute inflammation. Finally, we detected selectively decreased association of the transcription factors IFN consensus sequence binding protein and NF-kappaB with the IL-12p40 promoter in 12/15-LO-deficient macrophages. Taken together, these findings reveal a highly selective pathway to IL-12 production that may prove a useful target in chronic inflammation while sparing the acute response to infection. | lld:pubmed |
| pubmed-article:16365418 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16365418 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16365418 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16365418 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16365418 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16365418 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16365418 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16365418 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16365418 | pubmed:author | pubmed-author:PuréEllenE | lld:pubmed |
| pubmed-article:16365418 | pubmed:author | pubmed-author:MiddletonMeli... | lld:pubmed |
| pubmed-article:16365418 | pubmed:author | pubmed-author:RubinsteinTan... | lld:pubmed |
| pubmed-article:16365418 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16365418 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16365418 | pubmed:volume | 176 | lld:pubmed |
| pubmed-article:16365418 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16365418 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16365418 | pubmed:pagination | 265-74 | lld:pubmed |
| pubmed-article:16365418 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:16365418 | pubmed:meshHeading | pubmed-meshheading:16365418... | lld:pubmed |
| pubmed-article:16365418 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16365418 | pubmed:articleTitle | Cellular and molecular mechanisms of the selective regulation of IL-12 production by 12/15-lipoxygenase. | lld:pubmed |
| pubmed-article:16365418 | pubmed:affiliation | The Wistar Institute, Philadelphia, PA 19104, USA. | lld:pubmed |
| pubmed-article:16365418 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16365418 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16365418 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:11687 | entrezgene:pubmed | pubmed-article:16365418 | lld:entrezgene |
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