| pubmed-article:7527552 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7527552 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:7527552 | lifeskim:mentions | umls-concept:C1281743 | lld:lifeskim |
| pubmed-article:7527552 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:7527552 | pubmed:issue | 25 | lld:pubmed |
| pubmed-article:7527552 | pubmed:dateCreated | 1995-1-11 | lld:pubmed |
| pubmed-article:7527552 | pubmed:abstractText | To study the role of B-cell antigen CD40 in immune responses, mouse embryonic stem (ES) cells in which both copies of the gene encoding CD40 had been disrupted by homologous recombination were injected in RAG-2 (recombination-activating gene-2)-deficient blastocysts to generate chimeras in which all mature lymphocytes are derived from the CD40-deficient ES cells. T- and B-cell number and phenotype were normal in the CD40-/- chimeras. However, B cells failed to proliferate and undergo isotype switching in vitro in response to soluble CD40 ligand (sCD40L) with interleukin 4 (IL-4) but responded normally to lipopolysaccharide (LPS) with IL-4. CD40-/- chimeras completely failed to mount an antigen-specific antibody response or to develop germinal centers following immunization with the T cell-dependent (TD) antigen keyhole limpet hemocyanin. In contrast, CD40-/- mutant mice responded normally to the T cell-independent (TI) antigens, 2,4,6-trinitrophenyl (TNP)-LPS and TNP-Ficoll. The most noticeable alteration in the serum immunoglobulin levels of young (6-8 weeks old) CD40-/- animals was absence of IgE and severe decrease of IgG1 and IgG2a. These results confirm the essential role of CD40- CD40L interactions in the antibody response to TD antigens and in isotype switching. | lld:pubmed |
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| pubmed-article:7527552 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7527552 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7527552 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7527552 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:7527552 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:DavidsonLL | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:CastigliEE | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:GehaR SRS | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:YuHH | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:BhanA KAK | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:BottaroAA | lld:pubmed |
| pubmed-article:7527552 | pubmed:author | pubmed-author:MizoguchiEE | lld:pubmed |
| pubmed-article:7527552 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7527552 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:7527552 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:7527552 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7527552 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7527552 | pubmed:pagination | 12135-9 | lld:pubmed |
| pubmed-article:7527552 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:7527552 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7527552 | pubmed:articleTitle | CD40-deficient mice generated by recombination-activating gene-2-deficient blastocyst complementation. | lld:pubmed |
| pubmed-article:7527552 | pubmed:affiliation | Division of Immunology, Children's Hospital, Boston, MA. | lld:pubmed |
| pubmed-article:7527552 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7527552 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7527552 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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