pubmed-article:1636092 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1636092 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
pubmed-article:1636092 | lifeskim:mentions | umls-concept:C0023270 | lld:lifeskim |
pubmed-article:1636092 | lifeskim:mentions | umls-concept:C0030498 | lld:lifeskim |
pubmed-article:1636092 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:1636092 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:1636092 | lifeskim:mentions | umls-concept:C0870509 | lld:lifeskim |
pubmed-article:1636092 | pubmed:issue | 5069 | lld:pubmed |
pubmed-article:1636092 | pubmed:dateCreated | 1992-8-26 | lld:pubmed |
pubmed-article:1636092 | pubmed:abstractText | The course of infection with the protozoan parasite Leishmania is determined in part by their early replication in macrophages, the exclusive host cells for these organisms. Although factors contributing to the survival of Leishmania are not well understood, cytokines influence the course of infection. Transforming growth factor-beta (TGF-beta) is a multipotential cytokine with diverse effects on cells of the immune system, including down-regulation of certain macrophage functions. Leishmanial infection induced the production of active TGF-beta, both in vitro and in vivo. TGF-beta was important for determining in vivo susceptibility to experimental leishmanial infection. | lld:pubmed |
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pubmed-article:1636092 | pubmed:language | eng | lld:pubmed |
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pubmed-article:1636092 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1636092 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1636092 | pubmed:month | Jul | lld:pubmed |
pubmed-article:1636092 | pubmed:issn | 0036-8075 | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:TwardzikD RDR | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:ReedS GSG | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:BarralAA | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:Barral-NettoM... | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:SkeikyY AYA | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:EllingsworthL... | lld:pubmed |
pubmed-article:1636092 | pubmed:author | pubmed-author:BrownellC ECE | lld:pubmed |
pubmed-article:1636092 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1636092 | pubmed:day | 24 | lld:pubmed |
pubmed-article:1636092 | pubmed:volume | 257 | lld:pubmed |
pubmed-article:1636092 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1636092 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1636092 | pubmed:pagination | 545-8 | lld:pubmed |
pubmed-article:1636092 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:1636092 | pubmed:meshHeading | pubmed-meshheading:1636092-... | lld:pubmed |
pubmed-article:1636092 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1636092 | pubmed:articleTitle | Transforming growth factor-beta in leishmanial infection: a parasite escape mechanism. | lld:pubmed |
pubmed-article:1636092 | pubmed:affiliation | Federal University of Bahia School of Medicine, Brazil. | lld:pubmed |
pubmed-article:1636092 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1636092 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1636092 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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