Linked Life Data

7238900

Source:http://linkedlifedata.com/resource/pubmed/id/7238900

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1981-8-20
pubmed:abstractText
IgE was detected in increasing quantities in supernatants of cultured human blood mononuclear cells, with peak amounts being found in 7 to 12-day cultures. Inhibitors of protein synthesis or of cell division reduced IgE production. Significantly greater amounts of IgE were made by cells from patients with elevated serum IgE than by those from normal adults. Pokeweed mitogen caused modest (threefold) augmentation of IgE synthesis is normal control cultures but inhibited it in cultures from patients with elevated serum IgE. Co-culturing unfractionated mononuclear cells from some atopic patients with cells from normal people resulted in significant suppression of the expected amount of IgE synthesis but not of IgM or IgG production. This suggests that a suppressor cell population or function is present in normal adults that regulates B cell IgE synthesis and that patients with elevated IgE may be deficient in this function. Results of coculture studies with isolated T and B cell-enriched subpopulations support the possibility that such activity exists in normal T cell populations. The marked augmentation of IgE synthesis by patients' B cells when separated from their own T cells indicates that patients' T cells have some regulatory capacity, but control T cells were more potent in this regard.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-9446
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2167-70
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
In vitro studies of IgE synthesis by human blood mononuclear cells.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.