pubmed-article:9767434 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
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pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1299583 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0334094 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1335671 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1608386 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C1549571 | lld:lifeskim |
pubmed-article:9767434 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:9767434 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:9767434 | pubmed:dateCreated | 1998-12-15 | lld:pubmed |
pubmed-article:9767434 | pubmed:abstractText | Infection of mice with African trypanosomes leads to a severe immunosuppression, mediated by suppressor macrophages. Using ex vivo macrophage culture and in vivo cell transfer, it has been shown that nitric oxide (NO) is a potent effector product of these cells and causes both lymphocyte unresponsiveness and dyserythropoiesis. We explored the role of NO in vivo during trypanosome infection using mice with a disrupted interferon-gamma-receptor gene, which were unable to respond with macrophage activation and NO synthesis. These mice were less effective at controlling parasitaemia than the wild types, but showed an improved splenic T-cell responsiveness and reduced anaemia during the early stages of infection. The data indicate that, in the mouse, NO is a significant mediator of immunosuppression only in early infection. Beyond day 10 of infection, NO-independent mechanisms are of primary significance and the control of parasitaemia and T-cell responsiveness are not directly related. | lld:pubmed |
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pubmed-article:9767434 | pubmed:language | eng | lld:pubmed |
pubmed-article:9767434 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9767434 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9767434 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9767434 | pubmed:month | Aug | lld:pubmed |
pubmed-article:9767434 | pubmed:issn | 0019-2805 | lld:pubmed |
pubmed-article:9767434 | pubmed:author | pubmed-author:WilsonR ARA | lld:pubmed |
pubmed-article:9767434 | pubmed:author | pubmed-author:CoulsonP SPS | lld:pubmed |
pubmed-article:9767434 | pubmed:author | pubmed-author:SmythiesL ELE | lld:pubmed |
pubmed-article:9767434 | pubmed:author | pubmed-author:SternbergJ... | lld:pubmed |
pubmed-article:9767434 | pubmed:author | pubmed-author:MabbottN ANA | lld:pubmed |
pubmed-article:9767434 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9767434 | pubmed:volume | 94 | lld:pubmed |
pubmed-article:9767434 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9767434 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9767434 | pubmed:pagination | 476-80 | lld:pubmed |
pubmed-article:9767434 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:9767434 | pubmed:year | 1998 | lld:pubmed |
pubmed-article:9767434 | pubmed:articleTitle | African trypanosome infections in mice that lack the interferon-gamma receptor gene: nitric oxide-dependent and -independent suppression of T-cell proliferative responses and the development of anaemia. | lld:pubmed |
pubmed-article:9767434 | pubmed:affiliation | *Department of Zoology, University of Aberdeen, Aberdeen, UK. | lld:pubmed |
pubmed-article:9767434 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9767434 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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