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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001511,
umls-concept:C0004561,
umls-concept:C0063695,
umls-concept:C0064830,
umls-concept:C0078056,
umls-concept:C0079091,
umls-concept:C0079717,
umls-concept:C0162638,
umls-concept:C0209606,
umls-concept:C0282491,
umls-concept:C1292733,
umls-concept:C1416487,
umls-concept:C1704259,
umls-concept:C1705987
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pubmed:issue |
8
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pubmed:dateCreated |
1994-5-5
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pubmed:abstractText |
In the germinal center (GC), B cells are either selected to become memory cells or are eliminated through the process of programmed cell death. FDC which are intimately associated with the GC B cells are thought to be important in this selection process. Previously, we have shown that the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) and VLA-4 (CD49d)-VCAM-1 (CD106) adhesion pathways are involved in FDC-B cell interaction. In the present study, we have explored whether these adhesive interactions contribute to the process of B cell selection by studying the effects on apoptosis of GC B cells. Using FDC and B cells derived from human tonsils, we found that only B cells adherent to FDC remain viable: disruption of FDC-B-cell clusters with mAb against LFA-1 alpha (CD11a), VLA-4 (CD49d), ICAM-1 (CD54), or VCAM-1 (CD106) results in apoptosis of the B cells. Furthermore, we found that GC B cells, upon adhesion to plastic-coated purified ICAM-1 (CD54) or VCAM-1 (CD106), show diminished apoptosis. Importantly, we observed that, at low concentration, ICAM-1 (CD54) and VCAM-1 (CD106) act synergistically with anti-IgM, in inhibiting apoptosis. Together, our data strongly suggest that adhesion of B cells via the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) pathway and VLA-4 (CD49d)-VCAM-1 (CD106) pathway contributes to B cell selection.
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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/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Function-Associated...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Very Late Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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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 |
15
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pubmed:volume |
152
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3760-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:7511659-Apoptosis,
pubmed-meshheading:7511659-B-Lymphocytes,
pubmed-meshheading:7511659-Cell Adhesion,
pubmed-meshheading:7511659-Cell Adhesion Molecules,
pubmed-meshheading:7511659-Child,
pubmed-meshheading:7511659-Dendritic Cells,
pubmed-meshheading:7511659-Humans,
pubmed-meshheading:7511659-Intercellular Adhesion Molecule-1,
pubmed-meshheading:7511659-Lymphocyte Function-Associated Antigen-1,
pubmed-meshheading:7511659-Palatine Tonsil,
pubmed-meshheading:7511659-Receptors, Very Late Antigen,
pubmed-meshheading:7511659-Vascular Cell Adhesion Molecule-1
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pubmed:year |
1994
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pubmed:articleTitle |
Adhesion through the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) and the VLA-4 (CD49d)-VCAM-1 (CD106) pathways prevents apoptosis of germinal center B cells.
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pubmed:affiliation |
Department of Pathology, University of Amsterdam, The Netherlands.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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