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| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C0019764 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C0224522 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C0015980 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C1823153 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C2349976 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C1552644 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:9712805 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:9712805 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:9712805 | pubmed:dateCreated | 1998-10-2 | lld:pubmed |
| pubmed-article:9712805 | pubmed:abstractText | Infection of fibroblast-like synovial cells with Chlamydia trachomatis (serotype D strain IC Cal 8) in culture induced the secretion of beta interferon (IFN-beta). Chlamydial infection inhibited IFN-gamma-induced expression of HLA-DR antigen in the cells. Addition of IFN-beta antibody directly to infected cultures mitigated HLA-DR inhibition, suggesting involvement of produced IFN-beta. | lld:pubmed |
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| pubmed-article:9712805 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9712805 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9712805 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9712805 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9712805 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:9712805 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:9712805 | pubmed:author | pubmed-author:LehmannMM | lld:pubmed |
| pubmed-article:9712805 | pubmed:author | pubmed-author:HartmannMM | lld:pubmed |
| pubmed-article:9712805 | pubmed:author | pubmed-author:VogelsangHH | lld:pubmed |
| pubmed-article:9712805 | pubmed:author | pubmed-author:StraubeEE | lld:pubmed |
| pubmed-article:9712805 | pubmed:author | pubmed-author:GromLL | lld:pubmed |
| pubmed-article:9712805 | pubmed:author | pubmed-author:RödelJJ | lld:pubmed |
| pubmed-article:9712805 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9712805 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:9712805 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9712805 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9712805 | pubmed:pagination | 4491-5 | lld:pubmed |
| pubmed-article:9712805 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9712805 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9712805 | pubmed:articleTitle | Beta interferon is produced by Chlamydia trachomatis-infected fibroblast-like synoviocytes and inhibits gamma interferon-induced HLA-DR expression. | lld:pubmed |
| pubmed-article:9712805 | pubmed:affiliation | Institute of Medical Microbiology, Friedrich Schiller University of Jena, D-07743 Jena, Germany. Roedel@BACH.med.uni-jena.de | lld:pubmed |
| pubmed-article:9712805 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9712805 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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