| pubmed-article:8423106 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C0040840 | lld:lifeskim |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C0020852 | lld:lifeskim |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C1159762 | lld:lifeskim |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C0369247 | lld:lifeskim |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
| pubmed-article:8423106 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:8423106 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8423106 | pubmed:dateCreated | 1993-2-22 | lld:pubmed |
| pubmed-article:8423106 | pubmed:abstractText | Rabbit antisera to Leptospira interrogans, Borrelia hermsii, and Treponema phagedenis biotype Reiter, reactive to shared spirochetal antigens, failed to enhance phagocytosis of Treponema pallidum by macrophages, while immunoglobulin G to Treponema pallidum subsp. pertenue and Treponema paraluiscuniculi promoted phagocytosis. Opsonic antibodies are directed to pathogen-restricted, not shared spirochetal, antigens. | lld:pubmed |
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| pubmed-article:8423106 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8423106 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8423106 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8423106 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8423106 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:8423106 | pubmed:author | pubmed-author:LukehartS ASA | lld:pubmed |
| pubmed-article:8423106 | pubmed:author | pubmed-author:ShafferJ MJM | lld:pubmed |
| pubmed-article:8423106 | pubmed:author | pubmed-author:Baker-ZanderS... | lld:pubmed |
| pubmed-article:8423106 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8423106 | pubmed:volume | 61 | lld:pubmed |
| pubmed-article:8423106 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8423106 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8423106 | pubmed:pagination | 781-4 | lld:pubmed |
| pubmed-article:8423106 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:8423106 | pubmed:meshHeading | pubmed-meshheading:8423106-... | lld:pubmed |
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| pubmed-article:8423106 | pubmed:meshHeading | pubmed-meshheading:8423106-... | lld:pubmed |
| pubmed-article:8423106 | pubmed:meshHeading | pubmed-meshheading:8423106-... | lld:pubmed |
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| pubmed-article:8423106 | pubmed:meshHeading | pubmed-meshheading:8423106-... | lld:pubmed |
| pubmed-article:8423106 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8423106 | pubmed:articleTitle | Opsonization of Treponema pallidum is mediated by immunoglobulin G antibodies induced only by pathogenic treponemes. | lld:pubmed |
| pubmed-article:8423106 | pubmed:affiliation | Department of Medicine, University of Washington, Seattle 98195. | lld:pubmed |
| pubmed-article:8423106 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8423106 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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