Published 19 February 2002. doi:10.1084/jem.20011543
© Rockefeller University Press, 0022-1007/2002/2/461/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 4, February 18, 2002 461-472
Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptormediated Cell Activation
Danielle Lankar1,
Hélène Vincent-Schneider1,
Volker Briken1,
Takeaki Yokozeki1,
Graça Raposo2 and
Christian Bonnerot1
1 Institut National de la Sante et de la Recherche Medicale U520 INSERM, Institut Curie, 75005 Paris, France
2 Centre National de la Recherche Scientifique UMR144 CNRS, Institut Curie, 75005 Paris, France
Address correspondence to C. Bonnerot, U520 INSERM, Institut Curie, 12 rue Lhomond, 75005 Paris, France. Phone: 33-142-3464-36; Fax: 33-142-3464-38; E-mail: bonnerot{at}curie.fr
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 IIrestricted 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 chainMHC class II complexes in MVBs. A few hours after BcR engagement, cathepsin S activity increased, the p10 invariant chain disappeared, and MHC class IIpeptide 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.
Key Words: antigen presentation multivesicular body lysosome B lymphocyte antigen receptor

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