| pubmed-article:8568248 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0043406 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0123759 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0022688 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:8568248 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:8568248 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8568248 | pubmed:dateCreated | 1996-3-6 | lld:pubmed |
| pubmed-article:8568248 | pubmed:abstractText | Although Yersinia enterocolitica is extracellularly located in infected tissues, a specific T cell response is required to overcome infection. Recent work implicated that in contrast to Yersinia-susceptible BALB/c mice, C57BL/6 mice are Yersinia resistant due to the rapid development of a Yersinia-specific Th1 T cell response. This study focused on the role of IL-12 in Y. enterocolitica infections in both mouse strains. We found that C57BL/6 and BALB/c mice produced comparable quantities of IL-12 mRNA after Y. enterocolitica infection. Likewise, Yersinia-infected bone marrow macrophages from both mouse strains produced equal quantities of IL-12. Administration of neutralizing anti-IL-12 Abs abrogated resistance against yersiniae in either strain. In addition, administration of rIL-12 rendered BALB/c mice resistant to yersiniae, while this treatment was toxic to C57BL/6 mice. IL-12-mediated protection was partially dependent on IFN-gamma. Spleen cells from both strains of mice produced Yersinia-triggered IFN-gamma in an IL-12-dependent manner, although those from BALB/c mice produced 10-fold lesser quantities. Administration of rIL-12 in vivo increased Yersinia-induced IFN-gamma production by BALB/c spleen cells in vitro, but decreased IFN-gamma production by spleen cells from C57BL/6 mice. IL-10 was antagonistic to IL-12 only in BALB/c mice and inhibited Yersinia-triggered IFN-gamma production. In vivo depletion experiments revealed that IL-12 accounts for Yersinia-induced IFN-gamma production by both NK cells and CD4+ T cells, the latter of which are an essential source of IFN-gamma r while NK cell-derived IFN-gamma production can be compensated by other cells. In contrast to that in the spleen, IL-12 plays a minor role in protection against yersiniae in Peyer's patches after orogastric infection. In summary, our data suggest that IL-12 is rapidly induced by Y. enterocolitica infection and required for IFN-gamma production by NK cells as well by CD4+ T cells. Although BALB/c and C57BL/6 mice produced comparable quantities of IL-12, IFN-gamma production, and thus resistance to yersiniae, can be increased by exogenous IL-12 only in BALB/c, not in C57BL/6, mice. | lld:pubmed |
| pubmed-article:8568248 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8568248 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8568248 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:8568248 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8568248 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8568248 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8568248 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8568248 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8568248 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8568248 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:8568248 | pubmed:author | pubmed-author:BohnEE | lld:pubmed |
| pubmed-article:8568248 | pubmed:author | pubmed-author:AutenriethI... | lld:pubmed |
| pubmed-article:8568248 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8568248 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:8568248 | pubmed:volume | 156 | lld:pubmed |
| pubmed-article:8568248 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8568248 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8568248 | pubmed:pagination | 1458-68 | lld:pubmed |
| pubmed-article:8568248 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:8568248 | pubmed:meshHeading | pubmed-meshheading:8568248-... | lld:pubmed |
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| pubmed-article:8568248 | pubmed:meshHeading | pubmed-meshheading:8568248-... | lld:pubmed |
| pubmed-article:8568248 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8568248 | pubmed:articleTitle | IL-12 is essential for resistance against Yersinia enterocolitica by triggering IFN-gamma production in NK cells and CD4+ T cells. | lld:pubmed |
| pubmed-article:8568248 | pubmed:affiliation | Institute for Hygiene and Microbiology, Wurzburg University, Germany. | lld:pubmed |
| pubmed-article:8568248 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8568248 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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