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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2011-8-12
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pubmed:abstractText |
Continuous migration of B cells at the follicle contrasts with their stable arrest after encounter with antigen. Two main ligand/receptor pairs are involved in these cell behaviors: the chemokine CXCL13/chemokine receptor CXCR5 and antigen/BCR. Little is known regarding the interplay between CXCR5 and BCR signaling in the modulation of B-cell dynamics and its effect on B-cell activation. We used a 2-dimensional model to study B-cell migration and antigen recognition in real time, and found that BCR signaling strength alters CXCL13-mediated migration, leading to a heterogeneous B-cell behavior pattern. In addition, we demonstrate that CXCL13/CXCR5 signaling does not impair BCR-triggered immune synapse formation and that CXCR5 is excluded from the central antigen cluster. CXCL13/CXCR5 signaling enhances BCR-mediated B-cell activation in at least 2 ways: (1) it assists antigen gathering at the synapse by promoting membrane ruffling and lymphocyte function-associated antigen 1 (LFA-1)-supported adhesion, and (2) it allows BCR signaling integration in motile B cells through establishment of LFA-1-supported migratory junctions. Both processes require functional actin cytoskeleton and non-muscle myosin II motor protein. Therefore, the CXCL13/CXCR5 signaling effect on shaping B-cell dynamics is an effective mechanism that enhances antigen encounter and BCR-triggered B-cell activation.
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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/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Blr1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL13,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl13 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Green Fluorescent Proteins,
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/Myosin Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, B-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR5
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1528-0020
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
11
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pubmed:volume |
118
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1560-9
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pubmed:meshHeading |
pubmed-meshheading:21659539-Actins,
pubmed-meshheading:21659539-Animals,
pubmed-meshheading:21659539-B-Lymphocytes,
pubmed-meshheading:21659539-Cell Line, Tumor,
pubmed-meshheading:21659539-Cell Membrane,
pubmed-meshheading:21659539-Cell Movement,
pubmed-meshheading:21659539-Cells, Cultured,
pubmed-meshheading:21659539-Chemokine CXCL13,
pubmed-meshheading:21659539-Cytoskeleton,
pubmed-meshheading:21659539-Green Fluorescent Proteins,
pubmed-meshheading:21659539-Intercellular Adhesion Molecule-1,
pubmed-meshheading:21659539-Kinetics,
pubmed-meshheading:21659539-Lymphocyte Activation,
pubmed-meshheading:21659539-Lymphocyte Function-Associated Antigen-1,
pubmed-meshheading:21659539-Mice,
pubmed-meshheading:21659539-Mice, Inbred BALB C,
pubmed-meshheading:21659539-Mice, Inbred C57BL,
pubmed-meshheading:21659539-Mice, Knockout,
pubmed-meshheading:21659539-Mice, Transgenic,
pubmed-meshheading:21659539-Microscopy, Confocal,
pubmed-meshheading:21659539-Microscopy, Fluorescence, Multiphoton,
pubmed-meshheading:21659539-Myosin Type II,
pubmed-meshheading:21659539-Receptors, Antigen, B-Cell,
pubmed-meshheading:21659539-Receptors, CXCR5,
pubmed-meshheading:21659539-Signal Transduction
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pubmed:year |
2011
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pubmed:articleTitle |
CXCL13/CXCR5 signaling enhances BCR-triggered B-cell activation by shaping cell dynamics.
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pubmed:affiliation |
B Cell Dynamics Group, Department of Immunology and Oncology, Centro Nacional de Biotecnología/Consejo Superior de Investigaciones Científicas, Madrid, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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