| pubmed-article:10594698 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0001175 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0003069 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0039195 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C1749467 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0487637 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0376315 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0205269 | lld:lifeskim |
| pubmed-article:10594698 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:10594698 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10594698 | pubmed:dateCreated | 2000-2-3 | lld:pubmed |
| pubmed-article:10594698 | pubmed:abstractText | Interactions between B and CD4+ T cells are central to the pathogenesis of retrovirus-induced murine acquired immune deficiency virus (MAIDS). Prompted by previous work showing that treatment with cytotoxic T lymphocyte antigen 4 immunoglobulin (CTLA4Ig) partly inhibited the disease, we studied the course of infection in mice deficient for CD28-B7 interactions (mCTLA4-Hgamma1 transgenic mice). Despite a relative viral load identical to that of non-transgenic mice, the transgenic mice did not develop any of the major MAIDS symptoms (i.e. lymphoproliferation and immune anergy). The mCTLA4-Hgamma1 did not however, completely inhibit B-cell activation as indicated by a slight hypergammaglobulinaemia and microscopic blastic transformation. Absence of MAIDS in transgenic mice was associated with much lower levels of both interleukin-4 and interferon-gamma transcripts following viral infection. These results support the theory that the CD28/B7 costimulatory pathway is a critical determinant to MAIDS development. | lld:pubmed |
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| pubmed-article:10594698 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10594698 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10594698 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10594698 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:10594698 | pubmed:issn | 0019-2805 | lld:pubmed |
| pubmed-article:10594698 | pubmed:author | pubmed-author:LangRR | lld:pubmed |
| pubmed-article:10594698 | pubmed:author | pubmed-author:BoniverJJ | lld:pubmed |
| pubmed-article:10594698 | pubmed:author | pubmed-author:MoutschenMM | lld:pubmed |
| pubmed-article:10594698 | pubmed:author | pubmed-author:De LevalLL | lld:pubmed |
| pubmed-article:10594698 | pubmed:author | pubmed-author:DebrusSS | lld:pubmed |
| pubmed-article:10594698 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10594698 | pubmed:volume | 98 | lld:pubmed |
| pubmed-article:10594698 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10594698 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10594698 | pubmed:pagination | 630-8 | lld:pubmed |
| pubmed-article:10594698 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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