Linked Life Data

2365994

Source:http://linkedlifedata.com/resource/pubmed/id/2365994

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-8-14
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
549-55
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Evidence for an intrinsic B cell defect in lpr/lpr mice apparent in neonatal chimeras.
pubmed:affiliation
Department of Microbiology, Boston University School of Medicine, MA 02118.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.