Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1985-9-25
pubmed:abstractText
Reticuloendothelial Fc function was examined in 24 normal individuals by determining the clearance rates of erythrocytes coated with rhesus antibody (IgG RBC) or chemically modified by treatment with n-ethyl malemide (NEM). The mean clearance times for the IgG RBC (52.1 +/- 10.3 min) and the NEM cells (87.5 +/- 14.7 min) in the 10 individuals who possessed the HLA antigen DR3 did not differ significantly from the mean clearance times observed in the 14 non-DR3 controls (IgG RBC 51.5 +/- 6.9 min and NEM cells 77.6 +/- 4.5 min). Two individuals with prolonged clearance times for the IgG RBC were identified in each group, the values observed being 80, 103, 119 and 137 min. These prolonged clearance times could not be attributed to lower numbers of antibody molecules bound to the red cell surface. The prolonged clearance times were reproducible but the putative Fc receptor defect in these individuals could be abolished by using IgG RBC obtained from different donors. When IgG RBC, prepared from a single donor were used to assess Fc function, no difference in the clearance rates of DR3 positive and DR3 negative individuals was found. Our results indicate that differences in the distribution of the rhesus antigen on the red cell surface can markedly influence the fate of these cells in vivo. We suggest that this is the explanation for our failure to confirm the association between Fc receptor defects and the HLA antigen DR3.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0009-9104
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
532-8
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
Reticuloendothelial Fc function in normal individuals and its relationship to the HLA antigen DR3.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't