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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1991-4-22
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pubmed:abstractText |
The possible role of CD23 in the activation of human B lymphocytes was systematically investigated by examining the effect of: 1) anti-CD23 mAb; 2) IgE or IgE-immune complexes and; 3) native or recombinant soluble CD23 of different m.w., on B cell proliferation. Intact anti-CD23 mAb or its F(ab')2 fragments inhibit the proliferation of tonsillar B lymphocytes costimulated with either Staphylococcus aureus Cowan I (SAC) or anti-IgM and IL-4. The antibody has no effect when IL-2 or LMW-BCGF is used as the second stimulant. The response of IL-4-pretreated B cells (expressing high levels of CD23) to anti-IgM together with IL-2 or B cell-derived B cell growth factor is inhibited by anti-CD23 mAb, indicating that this antibody prevents B cell activation regardless of the B cell activators but provided that the density of CD23 on B cells is sufficient. Anti-CD23 mAb markedly inhibits DNA synthesis only when added during the first 12 h of the culture and has no effect on the ongoing proliferation of CD23-bearing B cell blasts (SAC induced and IL-4 supported or EBV transformed). Monovalent Fab fragments of anti-CD23 mAb are inactive unless they are used in tandem with goat anti-mouse Fab suggesting that the inhibition is due to cross-linking of surface CD23. Most interestingly, polymeric IgE or IgE-immune complexes have the same effect as anti-CD23 and moreover they inhibit IgM production by SAC and IL4-stimulated B cells. The inhibiting effect of IgE or of anti-CD23 mAb is not due to their neutralization of soluble CD23 because these failed to display B cell growth factor activity under various experimental conditions. It is concluded that IgE-immune complexes may regulate activation and differentiation of CD23-bearing surfaceIgM/surfaceIgD precursor B lymphocytes.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fc,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgE
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
146
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2122-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1826018-Antibodies, Monoclonal,
pubmed-meshheading:1826018-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:1826018-B-Lymphocytes,
pubmed-meshheading:1826018-Cell Differentiation,
pubmed-meshheading:1826018-Humans,
pubmed-meshheading:1826018-Immunoglobulin E,
pubmed-meshheading:1826018-Lymphocyte Activation,
pubmed-meshheading:1826018-Receptor Aggregation,
pubmed-meshheading:1826018-Receptors, Fc,
pubmed-meshheading:1826018-Receptors, IgE,
pubmed-meshheading:1826018-Solubility
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pubmed:year |
1991
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pubmed:articleTitle |
Cross-linking of CD23 antigen by its natural ligand (IgE) or by anti-CD23 antibody prevents B lymphocyte proliferation and differentiation.
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pubmed:affiliation |
University of Montreal, Notre-Dame Hospital, Research Center, Canada.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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