| pubmed-article:16051621 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C0004364 | lld:lifeskim |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C0812201 | lld:lifeskim |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C1423633 | lld:lifeskim |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C1155004 | lld:lifeskim |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C0181586 | lld:lifeskim |
| pubmed-article:16051621 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:16051621 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:16051621 | pubmed:dateCreated | 2005-8-23 | lld:pubmed |
| pubmed-article:16051621 | pubmed:abstractText | It has been shown that mice with a targeted mutation in the Ets-1 gene exhibit increased B cell terminal differentiation to IgM-secreting plasma cells. Here, we show that mice, formerly described to lack Ets-1 protein, actually express low levels of an internally deleted Ets-1 protein. Mice harboring this Ets-1 hypomorphic allele possess very few marginal zone B cells and have increased expression of activation markers on follicular B cells. Adoptive transfer experiments indicate that this activated phenotype can be reversed upon transfer of Ets-1-deficient B cells to a wild-type host, suggesting a role for B cell-extrinsic factors in regulating the activated state. Supporting this observation, the reverse transfer experiment of wild-type B cells into an Ets-1-deficient host resulted in increased expression of activation markers on the transferred B cells. However, there are also cell-intrinsic changes in Ets-1-deficient B cells as demonstrated by their increased differentiation to plasma cells in vitro in response to stimulation with cytosine-phosphate-guanine DNA sequence-containing oligodeoxynucleotide [CpG DNA, a Toll-like receptor (TLR) 9 ligand]. Consistent with the activated phenotype and increased terminal differentiation of Ets-1-deficient B cells, Ets-1 mutant mice develop autoimmune disease. Hence, our studies establish Ets-1 as an important regulator of peripheral B cell differentiation and B cell responses to TLR9 activation. | lld:pubmed |
| pubmed-article:16051621 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16051621 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16051621 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16051621 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16051621 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16051621 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16051621 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16051621 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16051621 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16051621 | pubmed:issn | 0953-8178 | lld:pubmed |
| pubmed-article:16051621 | pubmed:author | pubmed-author:JohnShinu ASA | lld:pubmed |
| pubmed-article:16051621 | pubmed:author | pubmed-author:WangDunchengD | lld:pubmed |
| pubmed-article:16051621 | pubmed:author | pubmed-author:ClementsJames... | lld:pubmed |
| pubmed-article:16051621 | pubmed:author | pubmed-author:Garrett-Sinha... | lld:pubmed |
| pubmed-article:16051621 | pubmed:author | pubmed-author:PercyDean HDH | lld:pubmed |
| pubmed-article:16051621 | pubmed:author | pubmed-author:BartonKevin... | lld:pubmed |
| pubmed-article:16051621 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16051621 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:16051621 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16051621 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16051621 | pubmed:pagination | 1179-91 | lld:pubmed |
| pubmed-article:16051621 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:16051621 | pubmed:meshHeading | pubmed-meshheading:16051621... | lld:pubmed |
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| pubmed-article:16051621 | pubmed:meshHeading | pubmed-meshheading:16051621... | lld:pubmed |
| pubmed-article:16051621 | pubmed:meshHeading | pubmed-meshheading:16051621... | lld:pubmed |
| pubmed-article:16051621 | pubmed:meshHeading | pubmed-meshheading:16051621... | lld:pubmed |
| pubmed-article:16051621 | pubmed:meshHeading | pubmed-meshheading:16051621... | lld:pubmed |
| pubmed-article:16051621 | pubmed:meshHeading | pubmed-meshheading:16051621... | lld:pubmed |
| pubmed-article:16051621 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16051621 | pubmed:articleTitle | Ets-1 deficiency leads to altered B cell differentiation, hyperresponsiveness to TLR9 and autoimmune disease. | lld:pubmed |
| pubmed-article:16051621 | pubmed:affiliation | Department of Biochemistry, State University of New York at Buffalo, 3435 Main Street, Buffalo, NY 14214, USA. | lld:pubmed |
| pubmed-article:16051621 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16051621 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:23871 | entrezgene:pubmed | pubmed-article:16051621 | lld:entrezgene |
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