pubmed-article:15961576 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C0021051 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C0024501 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:15961576 | lifeskim:mentions | umls-concept:C2826170 | lld:lifeskim |
pubmed-article:15961576 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:15961576 | pubmed:dateCreated | 2005-8-29 | lld:pubmed |
pubmed-article:15961576 | pubmed:abstractText | Our previous investigation of a patient (pt1) with non-X-linked hyper-immunoglobulin M syndrome revealed a CD40-mediated defect in B cell activation that resulted in low CD23 expression and absence of germ-line transcription and class-switch recombination. These deficiencies were complemented in vitro by a high threshold of sustained signaling through CD40. To further analyze the signaling defect in pt1 B cells, two types of Epstein-Barr virus lymphoblastoid cell lines (LCLs) were generated that either constitutively expressed the viral transforming protein latent membrane protein-1 (LMP1; pt1-LCL) or expressed it under the control of a tet-inducible promoter (pt1-LCL(tet)). Because LMP1 signals through the CD40 pathway, the pt1-LCL and pt1-LCL(tet) lines allow comparison of downstream functions in response to either constitutive LMP1 signals or regulated LMP1 and CD40 signals. Immortalized pt1-LCLs were initially CD23(lo)/CD38(hi) and reverted to a CD23(hi)/CD38(lo) phenotype upon extended growth in culture, suggesting that the CD40 defect was reversed by selection and/or constitutive expression of LMP1. In contrast, pt1-LCL(tet) cells retained the CD23(lo)/CD38(hi) phenotype after extended periods of culture and failed to up-regulate CD23 in response to CD40 signals. Analysis of pt1-LCL(tet) cells in response to the CD40 signals in the presence or absence of LMP1 revealed that mitogenic activation resulted only from LMP1 and not CD40, indicating a difference in the response of pt1 B cells to these two distinct signals. Together, these data demonstrate that the pt1-LCL(tet) cells maintain the CD40-related defect and provide a unique approach to study the independent effects of LMP1- and CD40-directed signals. | lld:pubmed |
pubmed-article:15961576 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:language | eng | lld:pubmed |
pubmed-article:15961576 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15961576 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15961576 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15961576 | pubmed:month | Sep | lld:pubmed |
pubmed-article:15961576 | pubmed:issn | 0741-5400 | lld:pubmed |
pubmed-article:15961576 | pubmed:author | pubmed-author:LuKristina... | lld:pubmed |
pubmed-article:15961576 | pubmed:author | pubmed-author:CoveyLori RLR | lld:pubmed |
pubmed-article:15961576 | pubmed:author | pubmed-author:DryerRebecca... | lld:pubmed |
pubmed-article:15961576 | pubmed:author | pubmed-author:SongCharlesC | lld:pubmed |
pubmed-article:15961576 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15961576 | pubmed:volume | 78 | lld:pubmed |
pubmed-article:15961576 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15961576 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15961576 | pubmed:pagination | 620-9 | lld:pubmed |
pubmed-article:15961576 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:15961576 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15961576 | pubmed:articleTitle | Maintenance of the CD40-related immunodeficient response in hyper-IgM B cells immortalized with a LMP1-regulated mini-EBV. | lld:pubmed |
pubmed-article:15961576 | pubmed:affiliation | Nelson Biological Laboratories, Rutgers, The State University of New Jersey, 604 Allison Road, Piscataway, NJ 08854, USA. | lld:pubmed |
pubmed-article:15961576 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15961576 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:15961576 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:15961576 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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