| pubmed-article:17379312 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C0056184 | lld:lifeskim |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C0332197 | lld:lifeskim |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
| pubmed-article:17379312 | lifeskim:mentions | umls-concept:C1516356 | lld:lifeskim |
| pubmed-article:17379312 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:17379312 | pubmed:dateCreated | 2007-5-8 | lld:pubmed |
| pubmed-article:17379312 | pubmed:abstractText | Mice prematurely expressing human CR2 (hCR2) in the B cell lineage have a defective B cell ontogeny and immune response. Our recent analysis of this phenotype suggested that signaling through hCR2 and presumably mouse CD19 on the B cell surface, during bone marrow development, could result in the observed changes in B cell function in these mice. To test this hypothesis, we back crossed hCR2(high) transgenic mice onto the CD19(-/-) background. CD19(-/-)hCR2(high) mice were found to possess even fewer mature B cells than their CD19(+/+)hCR2(high) littermates, demonstrating that loss of CD19 exacerbated the effects elicited through hCR2. This data suggests that CD19 provides a survival signal during B cell development in this model. Next, we examined if the removal of the main ligand for CR2, namely C3d, through back-crossing onto the C3(-/-) background could restore normal B cell development. However, we found only minor recovery in peripheral B cell numbers and no obvious change in function. This was despite a three-fold increase in the level of hCR2 expression on B cells isolated from the spleen or bone marrow of C3(-/-)hCR2(high) mice when compared with C3 sufficient littermates. These data demonstrate that hCR2 is integrated in mouse B cell signaling and that the downstream effects of hCR2 expression during early B cell development are partially but not completely due to interaction with C3 fragments and signaling through CD19 in the bone marrow environment. | lld:pubmed |
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| pubmed-article:17379312 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17379312 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17379312 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17379312 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17379312 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:17379312 | pubmed:issn | 0161-5890 | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:HolersV... | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:HaluszczakCat... | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:KulikLiudmila... | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:MarchbankKevi... | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:RossbachAndre... | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:TwohigJasonJ | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:ReuterJasonJ | lld:pubmed |
| pubmed-article:17379312 | pubmed:author | pubmed-author:BullMelanieM | lld:pubmed |
| pubmed-article:17379312 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17379312 | pubmed:volume | 44 | lld:pubmed |
| pubmed-article:17379312 | pubmed:owner | NLM | lld:pubmed |
