| pubmed-article:8514390 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C1817882 | lld:lifeskim |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:8514390 | lifeskim:mentions | umls-concept:C0026930 | lld:lifeskim |
| pubmed-article:8514390 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8514390 | pubmed:dateCreated | 1993-7-22 | lld:pubmed |
| pubmed-article:8514390 | pubmed:abstractText | The present study examined the role of endogenous gamma interferon (IFN-gamma) in the formation of granulomas in mice which had been given a single intravenous injection of glycolipid-containing mycolic acid (trehalose 2,3,6'-trimycolate) purified from cell walls of Rhodococcus aurantiacus (Gordona aurantiaca) (GaGM) in the form of liposome. The histological status of granuloma formation in the livers, spleens, and lungs of GaGM-injected mice was studied at weeks 1 through 5, and the titers of endogenous IFN-gamma in all of these organ extracts and in the sera were determined by enzyme-linked immunosorbent assay. The granulomas, composed of epithelioid cells, developed until 3 weeks postinjection, and thereafter the granulomas regressed. The production of endogenous IFN-gamma was biphasic, with an early phase detected at days 1 through 3 and a late phase detected at weeks 1 through 5. The latter peak of endogenous IFN-gamma production proceeded in parallel with granuloma formation. Both the areas of granulomas and titers of IFN-gamma in these organs were dependent on the doses of GaGM used for injection. The cells which produce endogenous IFN-gamma in the spleens appear within the granulomas. To study the role of endogenous IFN-gamma in granuloma formation, the in vivo administration of rat anti-mouse IFN-gamma monoclonal antibody was carried out. Anti-mouse IFN-gamma monoclonal antibody neutralized endogenous IFN-gamma and resulted in the suppression of the number of granulomas and the size of each granuloma. These findings suggest that biphasic production of endogenous IFN-gamma in the local lesions may be crucial to the formation and development of the granulomas. | lld:pubmed |
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| pubmed-article:8514390 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8514390 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8514390 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8514390 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8514390 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8514390 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:8514390 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:8514390 | pubmed:author | pubmed-author:MinagawaTT | lld:pubmed |
| pubmed-article:8514390 | pubmed:author | pubmed-author:NakanoKK | lld:pubmed |
| pubmed-article:8514390 | pubmed:author | pubmed-author:AsanoMM | lld:pubmed |
| pubmed-article:8514390 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8514390 | pubmed:volume | 61 | lld:pubmed |
| pubmed-article:8514390 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8514390 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8514390 | pubmed:pagination | 2872-8 | lld:pubmed |
| pubmed-article:8514390 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8514390 | pubmed:meshHeading | pubmed-meshheading:8514390-... | lld:pubmed |
| pubmed-article:8514390 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8514390 | pubmed:articleTitle | Endogenous gamma interferon is essential in granuloma formation induced by glycolipid-containing mycolic acid in mice. | lld:pubmed |
| pubmed-article:8514390 | pubmed:affiliation | Department of Microbiology, School of Medicine, Hokkaido University, Sapporo, Japan. | lld:pubmed |
| pubmed-article:8514390 | pubmed:publicationType | Journal Article | lld:pubmed |
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