| pubmed-article:10925275 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C0123759 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C0666963 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C1335671 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
| pubmed-article:10925275 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:10925275 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10925275 | pubmed:dateCreated | 2000-9-14 | lld:pubmed |
| pubmed-article:10925275 | pubmed:abstractText | IL-18 is a proinflammatory cytokine that enhances innate and specific Th1 immune responses. During microbial infections, IL-18 is produced by activated macrophages. IL-18 exerts its effects in synergy with IFN-alpha or IL-12 to induce IFN-gamma. Here we show that in human NK and T cells IFN-alpha and IL-12 strongly up-regulate mRNA expression of the IL-18R components, accessory protein-like (AcPL) and IL-1R-related protein (IL-1Rrp). In addition, IFN-alpha enhanced the expression of MyD88, an adaptor molecule involved in IL-18 signaling. Pretreatment of T cells with IFN-alpha or IL-12 enhanced IL-18-induced NF-kappaB activation and sensitized the cells to respond to lower concentrations of IL-18. AcPL and IL-1Rrp genes were strongly expressed in T cells polarized with IL-12, whereas in IL-4-polarized cells these genes were expressed at very low levels, indicating that AcPL and IL-1Rrp genes are preferentially expressed in Th1 cells. In conclusion, the results suggest that IFN-alpha and IL-12 enhance innate as well as Th1 immune response by inducing IL-18R expression. | lld:pubmed |
| pubmed-article:10925275 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10925275 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10925275 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10925275 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:10925275 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:10925275 | pubmed:author | pubmed-author:JulkunenII | lld:pubmed |
| pubmed-article:10925275 | pubmed:author | pubmed-author:SarenevaTT | lld:pubmed |
| pubmed-article:10925275 | pubmed:author | pubmed-author:MatikainenSS | lld:pubmed |
| pubmed-article:10925275 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10925275 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:10925275 | pubmed:volume | 165 | lld:pubmed |
| pubmed-article:10925275 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10925275 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10925275 | pubmed:pagination | 1933-8 | lld:pubmed |
| pubmed-article:10925275 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:10925275 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10925275 | pubmed:articleTitle | IFN-alpha and IL-12 induce IL-18 receptor gene expression in human NK and T cells. | lld:pubmed |
| pubmed-article:10925275 | pubmed:affiliation | Department of Virology, National Public Health Institute, Helsinki, Finland. | lld:pubmed |
| pubmed-article:10925275 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10925275 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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