| pubmed-article:2365994 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C0008109 | lld:lifeskim |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C0205102 | lld:lifeskim |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C1457869 | lld:lifeskim |
| pubmed-article:2365994 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:2365994 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:2365994 | pubmed:dateCreated | 1990-8-14 | lld:pubmed |
| pubmed-article:2365994 | pubmed:abstractText | Stem cells from a lpr/lpr mouse do not cause the lpr syndrome characteristic of unmanipulated MRL/lpr mice when injected into nonautoimmune neonatal mice. Instead, these neonatal chimeras gradually become markedly lymphopenic. As adults, only limited donor cell engraftment (approximately 5%) was evident as assessed by cell surface staining of H-2D or Thy-1 allelic markers. However, the relatively low number of lpr/lpr-derived B cells produced greater than 90% of the circulating IgG2a antibody and all detectable IgG2a anti-ssDNA autoantibody, indicating that lpr/lpr B cells express an intrinsic genetic defect resulting in hyper-IgG and autoantibody secretion. | lld:pubmed |
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| pubmed-article:2365994 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2365994 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2365994 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2365994 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:2365994 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2365994 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:2365994 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:2365994 | pubmed:author | pubmed-author:GlaserR MRM | lld:pubmed |
| pubmed-article:2365994 | pubmed:author | pubmed-author:Marshak-Roths... | lld:pubmed |
| pubmed-article:2365994 | pubmed:author | pubmed-author:PerkinsD LDL | lld:pubmed |
| pubmed-article:2365994 | pubmed:author | pubmed-author:MichaelsonJJ | lld:pubmed |
| pubmed-article:2365994 | pubmed:author | pubmed-author:MahonC ACA | lld:pubmed |
| pubmed-article:2365994 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2365994 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:2365994 | pubmed:volume | 145 | lld:pubmed |
| pubmed-article:2365994 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2365994 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2365994 | pubmed:pagination | 549-55 | lld:pubmed |
| pubmed-article:2365994 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:2365994 | pubmed:meshHeading | pubmed-meshheading:2365994-... | lld:pubmed |
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| pubmed-article:2365994 | pubmed:meshHeading | pubmed-meshheading:2365994-... | lld:pubmed |
| pubmed-article:2365994 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2365994 | pubmed:articleTitle | Evidence for an intrinsic B cell defect in lpr/lpr mice apparent in neonatal chimeras. | lld:pubmed |
| pubmed-article:2365994 | pubmed:affiliation | Department of Microbiology, Boston University School of Medicine, MA 02118. | lld:pubmed |
| pubmed-article:2365994 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2365994 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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