| pubmed-article:8617932 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8617932 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:8617932 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:8617932 | lifeskim:mentions | umls-concept:C0023690 | lld:lifeskim |
| pubmed-article:8617932 | lifeskim:mentions | umls-concept:C0020204 | lld:lifeskim |
| pubmed-article:8617932 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:8617932 | lifeskim:mentions | umls-concept:C1539081 | lld:lifeskim |
| pubmed-article:8617932 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:8617932 | pubmed:dateCreated | 1996-6-13 | lld:pubmed |
| pubmed-article:8617932 | pubmed:abstractText | The effect of ligation of CD40 on the proliferation and Ig secretion of a battery of human Ig-secreting hybridomas was examined to determine the regulatory activity of this surface molecule on B cells after initial activation. B cell hybridomas were generated by fusing activated peripheral blood B cells with SPAZ-4, a non-Ig-secreting fusion partner, and were cloned before analysis. All hybridomas expressed CD40 comparably. These hybridomas were stimulated with either recombinant baculovirus-expressed membrane-bound CD40L or a soluble murine CD40L/CD8 construct in the presence or the absence of various cytokines. Concentrations of CD40L that saturated 40 to 100% of CD40 induced initial homotypic aggregation followed by Fas (CD95)-independent apoptosis, with resultant decreases in growth and Ig secretion. Concentrations of CD40L that saturated 15 to 25% of CD40 also stimulated aggregation of all hybridomas. However, proliferation and Ig secretion of 9 of 13 IgM-secreting hybridomas, but none of 14 IgG- or IgA-secreting hybridomas, were enhanced by these concentrations of CD40L. These responses were independent of interactions mediated by the adhesion pair CD1la/CD18-CD54. These results indicate that the impact of CD40 ligation on human Ig-secreting hybridomas varies with the extent of CD40 engagement and depending on whether the hybridoma derived from an activated B cell that had previously undergone switch recombination. | lld:pubmed |
| pubmed-article:8617932 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8617932 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8617932 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8617932 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:8617932 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8617932 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8617932 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8617932 | pubmed:month | May | lld:pubmed |
| pubmed-article:8617932 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:8617932 | pubmed:author | pubmed-author:LipskyP EPE | lld:pubmed |
| pubmed-article:8617932 | pubmed:author | pubmed-author:GrammerA CAC | lld:pubmed |
| pubmed-article:8617932 | pubmed:author | pubmed-author:BergmanM CMC | lld:pubmed |
| pubmed-article:8617932 | pubmed:author | pubmed-author:AttrepJ FJF | lld:pubmed |
| pubmed-article:8617932 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8617932 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8617932 | pubmed:volume | 156 | lld:pubmed |
| pubmed-article:8617932 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8617932 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8617932 | pubmed:pagination | 3118-32 | lld:pubmed |
| pubmed-article:8617932 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:8617932 | pubmed:meshHeading | pubmed-meshheading:8617932-... | lld:pubmed |
| pubmed-article:8617932 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8617932 | pubmed:articleTitle | Ligation of CD40 influences the function of human Ig-secreting B cell hybridomas both positively and negatively. | lld:pubmed |
| pubmed-article:8617932 | pubmed:affiliation | Harold C. Simmons Arthritis Research Center, University of Texas Southwestern Medical Center, Dallas 75235, USA. | lld:pubmed |
| pubmed-article:8617932 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8617932 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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