SEARCH:   Advanced

Blood, 4 June 2009, Vol. 113, No. 23, pp. 5878-5886. Prepublished online as a Blood First Edition Paper on March 27, 2009; DOI 10.1182/blood-2009-01-198465. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2009-01-198465v1 113/23/5878    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Espeli, M. Articles by Schiff, C. Search for Related Content PubMed PubMed Citation Articles by Espeli, M. Articles by Schiff, C. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Impaired B-cell development at the pre-BII-cell stage in galectin-1–deficient mice due to inefficient pre-BII/stromal cell interactions Marion Espeli13,*, Stéphane J. C. Mancini13,*, Caroline Breton13, Françoise Poirier4, and Claudine Schiff13 1 Centre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, 2 Inserm U631, and 3 Centre National de la Recherche Scientifique (CNRS), UMR6102, Case 906, Marseille, France; and 4 Institut Jacques Monod, CNRS UMR 7592, Paris, France Activation of the pre-B-cell receptor (pre-BCR) in the bone marrow depends on both tonic and ligand-induced signaling and leads to pre-BII-cell proliferation and differentiation. Using normal mouse bone marrow pre-BII cells, we demonstrate that the ligand-induced pre-BCR activation depends on pre-BCR/galectin-1/integrin interactions leading to pre-BCR clustering at the pre-BII/stromal cell synapse. In contrast, heparan sulfates, shown to be pre-BCR ligands in mice, are not implicated in pre-BCR relocalization. Inhibition of pre-BCR/galectin-1/integrin interactions has functional consequences, since pre-BII-cell proliferation and differentiation are impaired in an in vitro B-cell differentiation assay, without affecting cellular apoptosis. Most strikingly, although galectin-1–deficient mice do not show an apparent B-cell phenotype, the kinetics of de novo B-cell reconstitution after hydroxyurea treatment indicates a specific delay in pre-BII-cell recovery due to a decrease in pre-BII-cell differentiation and proliferation. Thus, although it remains possible that the pre-BCR interacts with other ligands, these results highlight the role played by the stromal cell–derived galectin-1 for the efficient development of normal pre-BII cells and suggest the existence of pre-BII–specific stromal cell niches in normal bone marrow. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

	Copyright © 2009 by American Society of Hematology         Online ISSN: 1528-0020