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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1987-5-11
pubmed:abstractText
We have previously demonstrated that monoclonal anti-I-A/E antibodies inhibit B-cell responses to lipopolysaccharide (LPS). In the present report, the inhibitory effects were shown to be carried out directly on B cells, and to be totally independent of the LPS concentration used, thereby showing that antibodies do not mediate their effect through blocking of accessory cells or steric hindrance of LPS-receptors. Of the three different phases in B-cell activation/induction, proliferation, and maturation, induction was shown to be the most sensitive to inhibition by anti-I-A/E antibodies. Thus, kinetic studies showed that anti-I-A/E antibodies are only inhibitory for the first 16 h of LPS activation, after which B cells can no longer be inhibited by these antibodies. Class II MHC molecules appear, therefore, to be part of a membrane molecular complex which regulates delivery of activation signals to resting B cells. Since it was also shown that this time period corresponds approximately to the time required for B cells to express functional reactivity to growth factors, we suggest that anti-I-A/E antibodies act on resting B lymphocytes to inhibit mitogen-dependent induction of growth receptor expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0300-9475
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
225-34
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
The role of I-A/E molecules in B-lymphocyte activation. II. Mechanism of inhibition of the responses to lipopolysaccharide by anti-I-A/E antibodies.
pubmed:publicationType
Journal Article