| pubmed-article:11067930 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11067930 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:11067930 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:11067930 | lifeskim:mentions | umls-concept:C0024501 | lld:lifeskim |
| pubmed-article:11067930 | lifeskim:mentions | umls-concept:C0020966 | lld:lifeskim |
| pubmed-article:11067930 | lifeskim:mentions | umls-concept:C0040557 | lld:lifeskim |
| pubmed-article:11067930 | lifeskim:mentions | umls-concept:C1326203 | lld:lifeskim |
| pubmed-article:11067930 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:11067930 | pubmed:dateCreated | 2000-11-21 | lld:pubmed |
| pubmed-article:11067930 | pubmed:abstractText | The NF-kappaB family of transcription factors are involved in the regulation of innate and adaptive immune functions associated with resistance to infection. To assess the role of NF-kappaB(2) in the regulation of cell-mediated immunity, mice deficient in the NF-kappaB(2) gene (NF-kappaB(2)(-/-)) were challenged with the intracellular parasite Toxoplasma gondii. Resistance to this opportunistic pathogen is dependent on the production of IL-12, which is required for the development of innate NK cell and adaptive T cell responses dominated by the production of IFN-gamma necessary to control replication of this parasite. Although wild-type controls were resistant to T. gondii, NF-kappaB(2)(-/-) mice developed severe toxoplasmic encephalitis and succumbed to disease between 3 and 10 wk following infection. However, NF-kappaB(2) was not required for the ability of macrophages to produce IL-12 or to inhibit parasite replication and during the acute stage of infection, NF-kappaB(2)(-/-) mice had no defect in their ability to produce IL-12 or IFN-gamma and infection-induced NK cell responses appeared normal. In contrast, during the chronic phase of the infection, susceptibility of NF-kappaB(2)(-/-) mice to toxoplasmic encephalitis was associated with a reduced capacity of their splenocytes to produce IFN-gamma associated with a loss of CD4(+) and CD8(+) T cells. This loss of T cells correlated with increased levels of apoptosis and with elevated expression of the pro-apoptotic molecule Fas by T cells from infected NF-kappaB(2)(-/-) mice. Together, these results suggest a role for NF-kappaB(2) in the regulation of lymphocyte apoptosis and a unique role for this transcription factor in maintenance of T cell responses required for long-term resistance to T. gondii. | lld:pubmed |
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| pubmed-article:11067930 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11067930 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11067930 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:11067930 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11067930 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11067930 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11067930 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:AlexanderJJ | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:CraigLL | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:HunterC ACA | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:CaiGG | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:TaucPP | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:CaamañoJJ | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:VillegasE NEN | lld:pubmed |
| pubmed-article:11067930 | pubmed:author | pubmed-author:SpeirsKK | lld:pubmed |
| pubmed-article:11067930 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11067930 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11067930 | pubmed:volume | 165 | lld:pubmed |
| pubmed-article:11067930 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11067930 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11067930 | pubmed:pagination | 5720-8 | lld:pubmed |
| pubmed-article:11067930 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11067930 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11067930 | pubmed:articleTitle | Identification of a role for NF-kappa B2 in the regulation of apoptosis and in maintenance of T cell-mediated immunity to Toxoplasma gondii. | lld:pubmed |
| pubmed-article:11067930 | pubmed:affiliation | Medical Research Council Centre for Immune Regulation, School of Medicine, University of Birmingham, Edgbaston, Birmingham, United Kingdom. | lld:pubmed |
| pubmed-article:11067930 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11067930 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11067930 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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