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PLoS One. 2010 Feb 18;5(2):e9277. doi: 10.1371/journal.pone.0009277.

A role for S1P and S1P1 in immature-B cell egress from mouse bone marrow.

Author information

1
Department of Microbiology and Immunology, University of California San Francisco, San Francisco, California, United States of America. Joao.Pereira@ucsf.edu

Erratum in

  • PLoS One. 2010;5(3). doi: 10.1371/annotation/2ae645ec-9413-4f7d-b51f-eb0678fa2f1b.

Abstract

B lymphocyte egress from secondary lymphoid organs requires sphingosine-1-phosphate (S1P) and S1P receptor-1 (S1P1). However, whether S1P contributes to immature-B cell egress from the bone marrow (BM) has not been fully assessed. Here we report that in S1P- and S1P1-conditionally deficient mice, the number of immature-B cells in the BM parenchyma increased, while it decreased in the blood. Moreover, a slower rate of bromodeoxyuridine incorporation suggested immature-B cells spent longer in the BM of mice in which S1P1-S1P signaling was genetically or pharmacologically impaired. Transgenic expression of S1P1 in developing B cells was sufficient to mobilize pro- and pre-B cells from the BM. We conclude that the S1P1-S1P pathway contributes to egress of immature-B cells from BM, and that this mechanism is partially redundant with other undefined pathways.

PMID:
20174580
PMCID:
PMC2823786
DOI:
10.1371/journal.pone.0009277
[Indexed for MEDLINE]
Free PMC Article

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