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Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation
Antigen recognition by clonotypic B cell receptor (BcR) is the first step of B lymphocytes differentiation into plasmocytes. This B cell function is dependent on efficient major histocompatibility complex (MHC) class II–restricted presentation of BcR-bound antigens. In this work, we analyzed the sub...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193618/ https://www.ncbi.nlm.nih.gov/pubmed/11854359 http://dx.doi.org/10.1084/jem.20011543 |
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author | Lankar, Danielle Vincent-Schneider, Hélène Briken, Volker Yokozeki, Takeaki Raposo, Graça Bonnerot, Christian |
author_facet | Lankar, Danielle Vincent-Schneider, Hélène Briken, Volker Yokozeki, Takeaki Raposo, Graça Bonnerot, Christian |
author_sort | Lankar, Danielle |
collection | PubMed |
description | Antigen recognition by clonotypic B cell receptor (BcR) is the first step of B lymphocytes differentiation into plasmocytes. This B cell function is dependent on efficient major histocompatibility complex (MHC) class II–restricted presentation of BcR-bound antigens. In this work, we analyzed the subcellular mechanisms underlying antigen presentation after BcR engagement on B cells. In quiescent B cells, we found that MHC class II molecules mostly accumulated at the cell surface and in an intracellular pool of tubulovesicular structures, whereas H2-M molecules were mostly detected in distinct lysosomal compartments devoid of MHC class II. BcR stimulation induced the transient intracellular accumulation of MHC class II molecules in newly formed multivesicular bodies (MVBs), to which H2-M was recruited. The reversible downregulation of cathepsin S activity led to the transient accumulation of invariant chain–MHC class II complexes in MVBs. A few hours after BcR engagement, cathepsin S activity increased, the p10 invariant chain disappeared, and MHC class II–peptide complexes arrived at the plasma membrane. Thus, BcR engagement induced the transient formation of antigen-processing compartments, enabling antigen-specific B cells to become effective antigen-presenting cells. |
format | Text |
id | pubmed-2193618 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21936182008-04-14 Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation Lankar, Danielle Vincent-Schneider, Hélène Briken, Volker Yokozeki, Takeaki Raposo, Graça Bonnerot, Christian J Exp Med Original Article Antigen recognition by clonotypic B cell receptor (BcR) is the first step of B lymphocytes differentiation into plasmocytes. This B cell function is dependent on efficient major histocompatibility complex (MHC) class II–restricted presentation of BcR-bound antigens. In this work, we analyzed the subcellular mechanisms underlying antigen presentation after BcR engagement on B cells. In quiescent B cells, we found that MHC class II molecules mostly accumulated at the cell surface and in an intracellular pool of tubulovesicular structures, whereas H2-M molecules were mostly detected in distinct lysosomal compartments devoid of MHC class II. BcR stimulation induced the transient intracellular accumulation of MHC class II molecules in newly formed multivesicular bodies (MVBs), to which H2-M was recruited. The reversible downregulation of cathepsin S activity led to the transient accumulation of invariant chain–MHC class II complexes in MVBs. A few hours after BcR engagement, cathepsin S activity increased, the p10 invariant chain disappeared, and MHC class II–peptide complexes arrived at the plasma membrane. Thus, BcR engagement induced the transient formation of antigen-processing compartments, enabling antigen-specific B cells to become effective antigen-presenting cells. The Rockefeller University Press 2002-02-18 /pmc/articles/PMC2193618/ /pubmed/11854359 http://dx.doi.org/10.1084/jem.20011543 Text en Copyright © 2002, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Original Article Lankar, Danielle Vincent-Schneider, Hélène Briken, Volker Yokozeki, Takeaki Raposo, Graça Bonnerot, Christian Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation |
title | Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation |
title_full | Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation |
title_fullStr | Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation |
title_full_unstemmed | Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation |
title_short | Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation |
title_sort | dynamics of major histocompatibility complex class ii compartments during b cell receptor–mediated cell activation |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193618/ https://www.ncbi.nlm.nih.gov/pubmed/11854359 http://dx.doi.org/10.1084/jem.20011543 |
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