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B Cell Progenitors Are Arrested in Maturation but Have Intact VDJ Recombination in the Absence of Ig-α and Ig-β1

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Pelanda,  Roberta
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Braun,  Uschi
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Hobeika,  Elias
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Reth,  Michael
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Pelanda, R., Braun, U., Hobeika, E., Nussenzweig, M. C., & Reth, M. (2002). B Cell Progenitors Are Arrested in Maturation but Have Intact VDJ Recombination in the Absence of Ig-α and Ig-β1. Journal of Immunology, 169(2), 865-872.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-9626-0
Abstract
Ig-α and Ig-β mediate surface expression and signaling of diverse B cell receptor complexes on precursor, immature, and mature B cells. Their expression begins before that of the Ig chains in early progenitor B cells. In this study, we describe the generation of Ig-α-deficient mice and their comparative analysis to mice deficient for Ig-β, the membrane-IgM, and recombination-activating gene 2 to determine the requirement of Ig-α and Ig-β in survival and differentiation of pro-B cells. We find that in the absence of Ig-α, B cell development does not progress beyond the progenitor stage, similar to what is observed in humans lacking this molecule. However, neither in Ig-α- nor in Ig-β-deficient mice are pro-B cells impaired in V(D)J recombination, in the expression of intracellular Ig μ-chains, or in surviving in the bone marrow microenvironment. Finally, Ig-α and Ig-β are not redundant in their putative function, as pro-B cells from Ig-α and Ig-β double-deficient mice are similar to those from single-deficient animals in every aspect analyzed.