Source:http://linkedlifedata.com/resource/pubmed/id/17274001
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2007-2-8
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pubmed:abstractText |
It is becoming increasingly clear that the regulation of proliferation and differentiation of B cells to plasma cells involves the integration of a variety of intracellular signals provided by receptors of both the adaptive and innate immune system. The cross-linking of the surface molecule CD38 induces calcium mobilization, protein phosphorylation and NF-kappaB translocation into the nucleus, ultimately leading to proliferation and isotype switching toward IgG1. Here we describe (a) the effect on B cell activation of stimulating through both CD38 and Toll-like receptors 4, 7 and 9; and (b) that CD38 cross-linking increases the number of proliferating cells and the rate of proliferation in LPS-stimulated B cells by a Bruton's tyrosine kinase- and protein kinase C-dependent mechanism. In contrast, CD38 cross-linking reduces the number of cells committed to IgM plasma cell differentiation as measured by the number of CD138+ cells, antibody secretion, and the expression of PAX5, Bcl6 and Blimp-1. Since a putative ligand for CD38 is expressed by germinal center follicular dendritic cells, and CD38 expression is down-regulated in germinal center B cells, we speculate that CD38 might participate in the outcome of post-germinal center antibody responses.
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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, CD38,
http://linkedlifedata.com/resource/pubmed/chemical/Ccnd2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclins,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
358-67
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17274001-Animals,
pubmed-meshheading:17274001-Antigens, CD38,
pubmed-meshheading:17274001-B-Lymphocytes,
pubmed-meshheading:17274001-Blotting, Western,
pubmed-meshheading:17274001-Cell Differentiation,
pubmed-meshheading:17274001-Cell Proliferation,
pubmed-meshheading:17274001-Cyclin D2,
pubmed-meshheading:17274001-Cyclins,
pubmed-meshheading:17274001-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:17274001-Female,
pubmed-meshheading:17274001-Flow Cytometry,
pubmed-meshheading:17274001-Immunoglobulin M,
pubmed-meshheading:17274001-Lipopolysaccharides,
pubmed-meshheading:17274001-Lymphocyte Activation,
pubmed-meshheading:17274001-Mice,
pubmed-meshheading:17274001-Plasma Cells,
pubmed-meshheading:17274001-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17274001-Signal Transduction,
pubmed-meshheading:17274001-Toll-Like Receptors
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pubmed:year |
2007
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pubmed:articleTitle |
CD38 cross-linking enhances TLR-induced B cell proliferation but decreases IgM plasma cell differentiation.
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pubmed:affiliation |
Molecular Biomedicine Department, Centro de Investigación y de Estudios Avanzados del IPN, Mexico City, México.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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