pubmed-article:8918578 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8918578 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
pubmed-article:8918578 | lifeskim:mentions | umls-concept:C0041296 | lld:lifeskim |
pubmed-article:8918578 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:8918578 | lifeskim:mentions | umls-concept:C0178784 | lld:lifeskim |
pubmed-article:8918578 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
pubmed-article:8918578 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:8918578 | pubmed:dateCreated | 1996-12-12 | lld:pubmed |
pubmed-article:8918578 | pubmed:abstractText | Protective immunity against infection with Mycobacterium tuberculosis is imparted by T cells rather than antibodies, but B cells can play a role as antigen-presenting cells and in granuloma formation. We re-evaluated the role of B cells in the course of tuberculous infection in mu-chain knock-out (Ig-) mice. Surprisingly, the organs of M. tuberculosis-infected Ig- mice were found to have three- to eight-fold elevated counts of viable bacilli compared with normal littermates at 3-6 weeks post-infection. Splenic interferon-gamma responses to whole antigen were unimpaired, whilst proliferation to certain mycobacterial peptides was found to be diminished. However, bacille Calmette-Guérin (BCG) vaccination significantly reduced the infection in Ig- mice. The mechanisms by which B cells can influence primary tuberculous infection need further study. | lld:pubmed |
pubmed-article:8918578 | pubmed:language | eng | lld:pubmed |
pubmed-article:8918578 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8918578 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8918578 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:8918578 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8918578 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8918578 | pubmed:month | Nov | lld:pubmed |
pubmed-article:8918578 | pubmed:issn | 0009-9104 | lld:pubmed |
pubmed-article:8918578 | pubmed:author | pubmed-author:IvanyiJJ | lld:pubmed |
pubmed-article:8918578 | pubmed:author | pubmed-author:HarrisD PDP | lld:pubmed |
pubmed-article:8918578 | pubmed:author | pubmed-author:VordermeierH... | lld:pubmed |
pubmed-article:8918578 | pubmed:author | pubmed-author:Venkataprasad... | lld:pubmed |
pubmed-article:8918578 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8918578 | pubmed:volume | 106 | lld:pubmed |
pubmed-article:8918578 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8918578 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8918578 | pubmed:pagination | 312-6 | lld:pubmed |
pubmed-article:8918578 | pubmed:dateRevised | 2008-11-20 | lld:pubmed |
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pubmed-article:8918578 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8918578 | pubmed:articleTitle | Increase of tuberculous infection in the organs of B cell-deficient mice. | lld:pubmed |
pubmed-article:8918578 | pubmed:affiliation | MRC Clinical Sciences Centre, Hammersmith Hospital, London, UK. | lld:pubmed |
pubmed-article:8918578 | pubmed:publicationType | Journal Article | lld:pubmed |
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