rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
6438
|
pubmed:dateCreated |
1993-9-14
|
pubmed:abstractText |
In mice transgenic for an autoantibody, self-reactive B cells have been shown to be eliminated upon interaction with membrane-bound self-antigens in the periphery as well as in the bone marrow, suggesting that both immature and mature B cells are eliminated by multimerization of surface immunoglobulins (sIg). Activation of mature B cells by antigens may thus require a second signal that inhibits sIg-mediated apoptosis. Such a second signal is likely to be provided by T helper cells, because B-cell tolerance is more easily induced in the absence of T helper cells. To assess the molecular nature of the signal that inhibits sIg-mediated apoptosis, we used anti-IgM-induced apoptotic death of WEHI-231 B lymphoma cells as a model system. Here we report that the signal for abrogating sIg-mediated apoptosis is generated by association of the CD40L molecule on T cells with the CD40 molecule on WEHI-231 cells. T-cell help through CD40 may thus determine whether B cells are eliminated or activated upon interaction with antigens.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CD40 Ligand,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
|
pubmed:issn |
0028-0836
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
12
|
pubmed:volume |
364
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
645-8
|
pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7688865-Animals,
pubmed-meshheading:7688865-Antigens, CD,
pubmed-meshheading:7688865-Antigens, CD40,
pubmed-meshheading:7688865-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:7688865-Apoptosis,
pubmed-meshheading:7688865-B-Lymphocytes,
pubmed-meshheading:7688865-Base Sequence,
pubmed-meshheading:7688865-CD40 Ligand,
pubmed-meshheading:7688865-Cell Communication,
pubmed-meshheading:7688865-Humans,
pubmed-meshheading:7688865-Immunoglobulin M,
pubmed-meshheading:7688865-Membrane Glycoproteins,
pubmed-meshheading:7688865-Mice,
pubmed-meshheading:7688865-Mice, Transgenic,
pubmed-meshheading:7688865-Molecular Sequence Data,
pubmed-meshheading:7688865-Receptors, Antigen, B-Cell,
pubmed-meshheading:7688865-Signal Transduction,
pubmed-meshheading:7688865-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:7688865-Tumor Cells, Cultured
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pubmed:year |
1993
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pubmed:articleTitle |
B-cell apoptosis induced by antigen receptor crosslinking is blocked by a T-cell signal through CD40.
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pubmed:affiliation |
Department of Medical Chemistry, Kyoto University Faculty of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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