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Mol Biol Cell. 2015 Apr 1;26(7):1273-85. doi: 10.1091/mbc.E14-09-1373. Epub 2015 Jan 28.

Polarity protein Par3 controls B-cell receptor dynamics and antigen extraction at the immune synapse.

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INSERM U932, Institut Curie, Centre de Recherche, 75005 Paris, France.
INSERM U932, Institut Curie, Centre de Recherche, 75005 Paris, France Departamento de Biologia Celular y Molecular, Pontificia Universidad Catolica de Chile, 6513677 Santiago, Chile.
INSERM U932, Institut Curie, Centre de Recherche, 75005 Paris, France Facultad de Ciencias de la Salud, Universidad San Sebastián, 7510157 Santiago, Chile.
Cell and Tissue Imaging Core Facility (PICT-IBiSA) and Nikon Imaging Centre, Institut Curie, UMR144, Centre de Recherche, 75005 Paris, France.
Department of Pathology and Cell Biology, Columbia University, New York, NY 10032.
Genentech, San Francisco, CA 94080.
Université Paris Descartes, Sorbonne Paris Cité, CNRS UMR8250, 75270 Paris Cedex 06, France.


B-cell receptor (BCR) engagement with surface-tethered antigens leads to the formation of an immune synapse, which facilitates antigen uptake for presentation to T-lymphocytes. Antigen internalization and processing rely on the early dynein-dependent transport of BCR-antigen microclusters to the synapse center, as well as on the later polarization of the microtubule-organizing center (MTOC). MTOC repositioning allows the release of proteases and the delivery of MHC class II molecules at the synapse. Whether and how these events are coordinated have not been addressed. Here we show that the ancestral polarity protein Par3 promotes BCR-antigen microcluster gathering, as well as MTOC polarization and lysosome exocytosis, at the synapse by facilitating local dynein recruitment. Par3 is also required for antigen presentation to T-lymphocytes. Par3 therefore emerges as a key molecule in the coupling of the early and late events needed for efficient extraction and processing of immobilized antigen by B-cells.

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