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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
1995-11-22
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pubmed:abstractText |
The demise of B cell progenitors expressing functional IgM receptors for self appears to be the main mechanism by which B cell tolerance is accomplished. The genetic mechanisms that regulate the death process during this critical step of B cell development are still poorly understood. We have studied the regulation of apoptosis in WEHI-231 lymphoma cells after treatment with a panel of anti-IgM mAbs as an in vitro model of clonal B cell deletion. We showed that a product of bcl-x, Bcl-xL, can inhibit anti-IgM-induced apoptosis but not cell cycle arrest in a dose-dependent manner. Bcl-xL was efficient in protecting B cells from low but not high avidity anti-IgM mAbs. In contrast to that observed with Bcl-xL, CD40 stimulation was efficient in inhibiting both cell cycle arrest and apoptosis after IgM cross-linking regardless of the binding avidity of the anti-IgM Ab. Moreover, activation through IgM receptors but not CD40 induced up-regulation followed by rapid down-modulation of Bcl-xL. Thus, the capacity of Bcl-xL to modulate anti-IgM-induced apoptosis in WEHI-231 cells is highly dependent on the avidity of the Ab-IgM receptor interaction.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Anti-Idiotypic,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Bcl2l1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Constant Regions,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fc,
http://linkedlifedata.com/resource/pubmed/chemical/anti-IgM,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
155
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3830-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7561089-Animals,
pubmed-meshheading:7561089-Antibodies, Anti-Idiotypic,
pubmed-meshheading:7561089-Antibody Affinity,
pubmed-meshheading:7561089-Antigens, CD40,
pubmed-meshheading:7561089-Apoptosis,
pubmed-meshheading:7561089-B-Lymphocytes,
pubmed-meshheading:7561089-Cell Cycle,
pubmed-meshheading:7561089-Immunoglobulin Constant Regions,
pubmed-meshheading:7561089-Immunoglobulin M,
pubmed-meshheading:7561089-Lymphoma, B-Cell,
pubmed-meshheading:7561089-Mice,
pubmed-meshheading:7561089-Proto-Oncogene Proteins,
pubmed-meshheading:7561089-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:7561089-Receptors, Fc,
pubmed-meshheading:7561089-Signal Transduction,
pubmed-meshheading:7561089-Transfection,
pubmed-meshheading:7561089-Tumor Cells, Cultured,
pubmed-meshheading:7561089-bcl-X Protein
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pubmed:year |
1995
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pubmed:articleTitle |
Modulation of anti-IgM-induced B cell apoptosis by Bcl-xL and CD40 in WEHI-231 cells. Dissociation from cell cycle arrest and dependence on the avidity of the antibody-IgM receptor interaction.
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pubmed:affiliation |
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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