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Blood, 15 August 2006, Vol. 108, No. 4, pp. 1123-1128. Prepublished online as a Blood First Edition Paper on April 13, 2006; DOI 10.1182/blood-2006-01-0061. This Article Full Text Full Text (PDF) All Versions of this Article: 2006-01-0061v1 108/4/1123    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Liu, A. Articles by Cavazzana-Calvo, M. Search for Related Content PubMed PubMed Citation Articles by Liu, A. Articles by Cavazzana-Calvo, M. Related Collections Free Research Articles Plenary Papers Hematopoiesis Immunobiology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLENARY PAPERS Competition within the early B-cell compartment conditions B-cell reconstitution after hematopoietic stem cell transplantation in nonirradiated recipients Allen Liu, Christian A. J. Vosshenrich, Chantal Lagresle-Peyrou, Michele Malassis-Seris, Christophe Hue, Alain Fischer, James P. Di Santo, and Marina Cavazzana-Calvo From the Développement normal et pathologique du système immunitaire, Institut National de la Santé et de la Recherche Médicale (INSERM) U768–Site Necker–Enfants Malades, Paris; Faculté de Médecine Université René Descartes Paris V; Unité des Cytokines et Développement Lymphoïde, INSERM U668, Institut Pasteur, Paris; Biotherapy Department, Assistance Publique–Hopitaux de Paris, Hôpital Necker–Enfants Malades, Paris; Unité d'Immuno-Hématologie Pédiatrique, Département de Pédiatrie, Hôpital Necker–Enfants Malades, Paris, France. Severe combined immunodeficiency (SCID) is characterized by a complete block in T-lymphocyte differentiation. Most SCID also affects B-cell development or function, although a normal pool of pro–B cells is detectable. Treatment of SCID consists of allogeneic hematopoietic stem cell transplantation (HSCT), but in the absence of a myeloablative conditioning regimen, only T cells, and in some cases, natural killer (NK) cells, are of donor origin, while all other leukocytes subsets are of host origin. We hypothesized that donor B-cell development success could be conditioned by the competitive ability of recipient B-cell precursors in the bone marrow. We therefore compared the outcome of unconditioned HSCT in mice that differed with respect to their pro–B-cell compartments. B-cell reconstitution was limited in recipient mice containing a normal pro–B-cell pool, whereas immature and mature B-cell numbers reached wild-type levels in mice with compromised early B-cell precursors. Interestingly, host NK cells did not modify the outcome of unconditioned HSCT as long as the early B-cell compartment was compromised. These observations suggest that recipient B-cell precursors condition the reconstitution of the donor B-cell pool and, if extrapolative to humans, suggest that conditioning regimens targeting host pro–B cells may help improve B-cell reconstitution after allogeneic HSCT. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Battling bone marrow B-lineage cells Tucker W. LeBien Blood 2006 108: 1120. [Full Text] [PDF] This article has been cited by other articles: K. H. T. Paraiso, T. Ghansah, A. Costello, R. W. Engelman, and W. G. Kerr Induced SHIP Deficiency Expands Myeloid Regulatory Cells and Abrogates Graft-versus-Host Disease J. Immunol., March 1, 2007; 178(5): 2893 - 2900. [Abstract] [Full Text] [PDF] G. Mostoslavsky, A. J. Fabian, S. Rooney, F. W. Alt, and R. C. Mulligan Complete correction of murine Artemis immunodeficiency by lentiviral vector-mediated gene transfer PNAS, October 31, 2006; 103(44): 16406 - 16411. [Abstract] [Full Text] [PDF]

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