| pubmed-article:8973614 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8973614 | lifeskim:mentions | umls-concept:C0010416 | lld:lifeskim |
| pubmed-article:8973614 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:8973614 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
| pubmed-article:8973614 | lifeskim:mentions | umls-concept:C0520990 | lld:lifeskim |
| pubmed-article:8973614 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:8973614 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:8973614 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8973614 | pubmed:dateCreated | 1997-1-21 | lld:pubmed |
| pubmed-article:8973614 | pubmed:abstractText | We investigated the role of TNF-alpha in the host defence mechanism against infection with a virulent strain of Cryptococcus neoformans. Administration of exogenous recombinant human TNF-alpha significantly prolonged the survival time of mice infected by intratracheal instillation of the organism. Surprisingly, neutralizing MoAb to murine TNF-alpha did not shorten their survival time, a finding inconsistent with previous results. To investigate the cause of this inconsistency, we examined the production of TNF-alpha in the lungs of infected mice. During the course of cryptococcosis, there was little or no generation of TNF-alpha mRNA in the lung. This might be partly due to a direct inhibitory action of the fungal microorganism of TNF-alpha production by macrophages. In vitro production of TNF-alpha by murine interferon-gamma (IFN-gamma)- and lipopolysaccharide (LPS)-stimulated macrophages was strongly inhibited by co-culturing with the whole yeast cells. In contrast, administration of recombinant murine IL-12 markedly induced TNF-alpha production and the neutralizing anti-TNF-alpha MoAb strongly blocked IL-12-induced protection of mice against cryptococcal infection. These results indicate that endogenously synthesized TNF-alpha has the potential to contribute to the elimination of C. neoformans and partly mediates the protective effect of IL-12. | lld:pubmed |
| pubmed-article:8973614 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8973614 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8973614 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8973614 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8973614 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8973614 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:8973614 | pubmed:author | pubmed-author:SaitoAA | lld:pubmed |
| pubmed-article:8973614 | pubmed:author | pubmed-author:TohyamaMM | lld:pubmed |
| pubmed-article:8973614 | pubmed:author | pubmed-author:KawakamiKK | lld:pubmed |
| pubmed-article:8973614 | pubmed:author | pubmed-author:QureshiM HMH | lld:pubmed |
| pubmed-article:8973614 | pubmed:author | pubmed-author:QifengXX | lld:pubmed |
| pubmed-article:8973614 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8973614 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:8973614 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8973614 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8973614 | pubmed:pagination | 468-74 | lld:pubmed |
| pubmed-article:8973614 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8973614 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8973614 | pubmed:articleTitle | Contribution of tumour necrosis factor-alpha (TNF-alpha) in host defence mechanism against Cryptococcus neoformans. | lld:pubmed |
| pubmed-article:8973614 | pubmed:affiliation | First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan. | lld:pubmed |
| pubmed-article:8973614 | pubmed:publicationType | Journal Article | lld:pubmed |
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