pubmed-article:1537373 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0041221 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0599739 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0024426 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0162388 | lld:lifeskim |
pubmed-article:1537373 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:1537373 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:1537373 | pubmed:dateCreated | 1992-4-1 | lld:pubmed |
pubmed-article:1537373 | pubmed:abstractText | Intracellular replication of the protozoan parasite Trypanosoma cruzi inside macrophages is essential for the production of the disease and the development of the parasite. Two CD4+ T cell lines, A10 and A28, were established from T. cruzi-infected BALB/c mice which specifically proliferated to parasite antigens. The trypanocidal activity of BALB/c macrophages was induced upon culture with the A10, but not with the A28 T cell line. The cell-free supernatant from this A10 line, as well as from immune spleen cells stimulated with specific antigen or concanavalin A, but not from the A28 T cell line also activated the trypanocidal activity of peritoneal macrophages or of the J774 macrophage-like cell line. when the lymphokine content of the supernatants from both cell lines was analyzed, it was found that the A10 T cell line secreted interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and interleukin 2, whereas the A28 line did not secrete IFN-gamma upon stimulation. Furthermore, the trypanocidal-inducing ability of A10 supernatant was completely abrogated by neutralizing anti-IFN-gamma antibodies and partially abrogated by neutralizing anti-TNF-alpha antibodies. When recombinant cytokines were added to J774 cells, IFN-gamma was able to induce significant trypanocidal activity whereas TNF-alpha was almost ineffective. However, TNF-alpha or lipopolysaccharide (LPS) showed a synergistic effect with IFN-gamma on macrophage activation. IFN-gamma triggered nitric oxide (NO) synthesis by J774 cells whereas TNF-alpha was almost ineffective. TNF-alpha and LPS were also synergistic with IFN-gamma in the NO production. Both the NO production and the trypanocidal activity in J774 cells induced by T cell supernatants or lymphokine combinations were inhibited by N-monomethyl-L-arginine, a competitive inhibitor of NO synthase activity. A good correlation between the levels of NO production and trypanocidal activity induced by different lymphokine preparations was found. Those results suggest that IFN-gamma and TNF-alpha, secreted by T. cruzi-immune T cells, are involved in the activation of the trypanocidal activity of mouse macrophages through an NO-dependent mechanism. | lld:pubmed |
pubmed-article:1537373 | pubmed:language | eng | lld:pubmed |
pubmed-article:1537373 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1537373 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1537373 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1537373 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:1537373 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1537373 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1537373 | pubmed:month | Feb | lld:pubmed |
pubmed-article:1537373 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:1537373 | pubmed:author | pubmed-author:FresnoMM | lld:pubmed |
pubmed-article:1537373 | pubmed:author | pubmed-author:FernándezM... | lld:pubmed |
pubmed-article:1537373 | pubmed:author | pubmed-author:Muñoz-Fernánd... | lld:pubmed |
pubmed-article:1537373 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1537373 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:1537373 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1537373 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1537373 | pubmed:pagination | 301-7 | lld:pubmed |
pubmed-article:1537373 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
pubmed-article:1537373 | pubmed:meshHeading | pubmed-meshheading:1537373-... | lld:pubmed |
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pubmed-article:1537373 | pubmed:meshHeading | pubmed-meshheading:1537373-... | lld:pubmed |
pubmed-article:1537373 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1537373 | pubmed:articleTitle | Synergism between tumor necrosis factor-alpha and interferon-gamma on macrophage activation for the killing of intracellular Trypanosoma cruzi through a nitric oxide-dependent mechanism. | lld:pubmed |
pubmed-article:1537373 | pubmed:affiliation | Centro de Biología Molecular, CSIC-UAM Universidad Autónoma de Madrid, Spain. | lld:pubmed |
pubmed-article:1537373 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1537373 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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