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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
7
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pubmed:dateCreated |
2001-7-12
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pubmed:abstractText |
Following stimulation, primary B cells either directly undergo terminal differentiation to IgM-secreting plasma cells or enter the memory pathway characterized by affinity maturation and isotype switching. Which of the various fates is adopted by B cells is determined by the strength and duration of the antigenic signal, the availability and quality of T cell help and additional signals derived from the germinal center milieu. High rate secretion is correlated with endogenous Blimp-1 levels and can be caused by ectopic expression of Blimp-1. Using cultures of resting primary mouse B cells stimulated in vitro in various combinations with IL-4, anti-mu F(ab')2 or anti-CD40 in the absence or presence of lipopolysaccharide, we show that IgM secretion and the expression of Blimp-1 is either not induced or even suppressed by B cell receptors (BCR) or CD40 ligation and by IL-4. Additional treatment with IL-2 and IL-5 induces Blimp-1 expression and facilitates IgM and IgG1 secretion, which can also be achieved by retroviral transduction of Blimp-1. On the other hand, the drastic increase in membrane IgG1(+) cells with time in cultures treated with IL-4 is greatly diminished in cells forced to express Blimp-1. We conclude that suppression of Blimp-1 by antigen-BCR interaction and T helper cell-dependent CD40 and IL-4 signaling are necessary to facilitate entrance into the memory pathway and to prevent terminal differentiation.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-5,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Prdm1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1972-80
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11449349-Animals,
pubmed-meshheading:11449349-Antigens, CD40,
pubmed-meshheading:11449349-B-Lymphocytes,
pubmed-meshheading:11449349-Cell Differentiation,
pubmed-meshheading:11449349-Cell Line,
pubmed-meshheading:11449349-Cells, Cultured,
pubmed-meshheading:11449349-Immunoglobulin Class Switching,
pubmed-meshheading:11449349-Immunoglobulin G,
pubmed-meshheading:11449349-Immunoglobulin M,
pubmed-meshheading:11449349-Interleukin-2,
pubmed-meshheading:11449349-Interleukin-4,
pubmed-meshheading:11449349-Interleukin-5,
pubmed-meshheading:11449349-Lipopolysaccharides,
pubmed-meshheading:11449349-Mice,
pubmed-meshheading:11449349-Mice, Inbred C57BL,
pubmed-meshheading:11449349-Models, Immunological,
pubmed-meshheading:11449349-RNA, Messenger,
pubmed-meshheading:11449349-Repressor Proteins,
pubmed-meshheading:11449349-Transcription Factors,
pubmed-meshheading:11449349-Up-Regulation
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pubmed:year |
2001
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pubmed:articleTitle |
Blimp-1 over-expression abrogates IL-4- and CD40-mediated suppression of terminal B cell differentiation but arrests isotype switching.
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pubmed:affiliation |
Institute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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