pubmed-article:8543815 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C0040558 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C1298908 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
pubmed-article:8543815 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
pubmed-article:8543815 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:8543815 | pubmed:dateCreated | 1996-2-14 | lld:pubmed |
pubmed-article:8543815 | pubmed:abstractText | Production of nitric oxide (NO) by macrophages is important for the killing of intracellular pathogens. IFN-gamma and LPS stimulate NO production by transcriptional up-regulation of inducible nitric oxide synthetase (iNOS). In the present study we used mice with a targeted disruption of the IFN regulatory factor-1 gene (IRF-1-/-) to investigate the importance of NO in the host immune response against Toxoplasma gondii, a major cause of infection in newborns and those with AIDS. IRF-1-/- mice were more susceptible to acute Toxoplasma infection, and treatment with either exogenous IFN-gamma or in vivo neutralization of endogenous IFN-gamma had little effect on their susceptibility to infection. However, administration of exogenous IL-12 was able to prolong survival even when IFN-gamma was depleted. An in vivo depletion study suggested that the mechanism of this protective response is mediated in part by CD4+ T cells. The administration of IL-12 could not overcome the inhibition of lymphoproliferative response in T. gondii-infected mice and treatment with N-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase (iNOS) antagonist in vitro was unable to reverse the immunosuppression. In response to Toxoplasma infection, splenocytes from IRF-1-/- mice exhibited increased production of IL-10 as well as a 30-fold increase in its message expression. These studies indicate that NO may not be essential for host immunity to the parasite, and moreover that IL-12 appears to induce an IFN-gamma-independent mechanism of protection against this opportunistic pathogen. | lld:pubmed |
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pubmed-article:8543815 | pubmed:language | eng | lld:pubmed |
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pubmed-article:8543815 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:8543815 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8543815 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8543815 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8543815 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8543815 | pubmed:month | Jan | lld:pubmed |
pubmed-article:8543815 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:8543815 | pubmed:author | pubmed-author:MatsuuraTT | lld:pubmed |
pubmed-article:8543815 | pubmed:author | pubmed-author:KasperL HLH | lld:pubmed |
pubmed-article:8543815 | pubmed:author | pubmed-author:KhanI AIA | lld:pubmed |
pubmed-article:8543815 | pubmed:author | pubmed-author:FonsekaSS | lld:pubmed |
pubmed-article:8543815 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8543815 | pubmed:day | 15 | lld:pubmed |
pubmed-article:8543815 | pubmed:volume | 156 | lld:pubmed |
pubmed-article:8543815 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8543815 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8543815 | pubmed:pagination | 636-43 | lld:pubmed |
pubmed-article:8543815 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:8543815 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8543815 | pubmed:articleTitle | Production of nitric oxide (NO) is not essential for protection against acute Toxoplasma gondii infection in IRF-1-/- mice. | lld:pubmed |
pubmed-article:8543815 | pubmed:affiliation | Department of Medicine, Dartmouth Medical School, Hanover, NH 03755, USA. | lld:pubmed |
pubmed-article:8543815 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8543815 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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