pubmed-article:12756267 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C0079784 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C0018183 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C0597722 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C1317973 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C0183683 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C0344211 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C1521721 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C0439836 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C1518071 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C1881379 | lld:lifeskim |
pubmed-article:12756267 | lifeskim:mentions | umls-concept:C1171411 | lld:lifeskim |
pubmed-article:12756267 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:12756267 | pubmed:dateCreated | 2003-5-20 | lld:pubmed |
pubmed-article:12756267 | pubmed:abstractText | We evaluated the effects of ectopic granulocyte/macrophage colony-stimulating factor (GM-CSF) signals on hematopoietic commitment and differentiation. Lineage-restricted progenitors purified from mice with the ubiquitous transgenic human GM-CSF receptor (hGM-CSFR) were used for the analysis. In cultures with hGM-CSF alone, hGM-CSFR-expressing (hGM-CSFR+) granulocyte/monocyte progenitors (GMPs) and megakaryocyte/erythrocyte progenitors (MEPs) exclusively gave rise to granulocyte/monocyte (GM) and megakaryocyte/erythroid (MegE) colonies, respectively, providing formal proof that GM-CSF signals support the GM and MegE lineage differentiation without affecting the physiological myeloid fate. hGM-CSFR transgenic mice were crossed with mice deficient in interleukin (IL)-7, an essential cytokine for T and B cell development. Administration of hGM-CSF in these mice could not restore T or B lymphopoiesis, indicating that enforced GM-CSF signals cannot substitute for IL-7 to promote lymphopoiesis. Strikingly, >50% hGM-CSFR+ common lymphoid progenitors (CLPs) and >20% hGM-CSFR+ pro-T cells gave rise to granulocyte, monocyte, and/or myeloid dendritic cells, but not MegE lineage cells in the presence of hGM-CSF. Injection of hGM-CSF into mice transplanted with hGM-CSFR+ CLPs blocked their lymphoid differentiation, but induced development of GM cells in vivo. Thus, hGM-CSF transduces permissive signals for myeloerythroid differentiation, whereas it transmits potent instructive signals for the GM differentiation to CLPs and early T cell progenitors. These data suggest that a majority of CLPs and a fraction of pro-T cells possess plasticity for myelomonocytic differentiation that can be activated by ectopic GM-CSF signals, supporting the hypothesis that the down-regulation of GM-CSFR is a critical event in producing cells with a lymphoid-restricted lineage potential. | lld:pubmed |
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pubmed-article:12756267 | pubmed:language | eng | lld:pubmed |
pubmed-article:12756267 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12756267 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12756267 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:12756267 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12756267 | pubmed:month | May | lld:pubmed |
pubmed-article:12756267 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:12756267 | pubmed:author | pubmed-author:WatanabeSumik... | lld:pubmed |
pubmed-article:12756267 | pubmed:author | pubmed-author:IwasakiHiromi... | lld:pubmed |
pubmed-article:12756267 | pubmed:author | pubmed-author:AkashiKoichiK | lld:pubmed |
pubmed-article:12756267 | pubmed:author | pubmed-author:Iwasaki-AraiJ... | lld:pubmed |
pubmed-article:12756267 | pubmed:author | pubmed-author:MiyamotoToshi... | lld:pubmed |
pubmed-article:12756267 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12756267 | pubmed:day | 19 | lld:pubmed |
pubmed-article:12756267 | pubmed:volume | 197 | lld:pubmed |
pubmed-article:12756267 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12756267 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12756267 | pubmed:pagination | 1311-22 | lld:pubmed |