S1P1 receptor directs the release of immature B cells from bone marrow into blood

Allende, María L.; Tuymetova, Galina; Lee, Bridgin G.; Bonifacino, Eliana; Wu, Yiming; Proia, Richard L.

doi:10.1084/jem.20092210

Cited by 153 publications

(156 citation statements)

References 60 publications

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“…1D). The number of CD93 (C1qR1)-expressing B cells, which are recognized as B cells recently released from the bone marrow (Allende et al, 2010;Pereira et al, 2009), was significantly increased in both spleen and peripheral blood (Fig. 1D).…”

Section: Hemorrhagic and Hemolytic Anemia Induce Rapid Release Of Devmentioning

confidence: 99%

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Ito

Hamazaki

Takaori‐Kondo³

et al. 2017

Cell Struct. Funct.

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ABSTRACT. Bone marrow stromal cells, including endothelial cells and mesenchymal stromal cells, support the maintenance, differentiation, and retention of hematopoietic stem and precursor cells under steady state conditions. At the onset of an emergency, such as severe blood loss or infection, the status of hematopoiesis in the bone marrow changes rapidly to ensure efficient production of cells of specific lineages; however, the function of stromal cells in emergency hematopoiesis has not been fully elucidated. Here, we unexpectedly found that B precursor, mature B, and T cells were released from the bone marrow into the blood circulation in the early phase of hemorrhagic anemia and phenylhydrazine-induced hemolytic anemia. Administration of erythropoietin, which normally increases in response to anemia, stimulated the egress of IgD low immature B cells and recirculating mature B cells, which usually reside in the perivascular and intravascular space, from the bone marrow within 24 h. We also observed that endothelial cells in the bone marrow expressed erythropoietin receptor, and the expression levels were higher than those in other tissues. Erythropoietin stimulation of bone marrow endothelial cells induced the phosphorylation of STAT5 in vitro. Moreover, in vivo treatment with erythropoietin decreased surface VCAM1 expression and Cxcl12 transcription in bone marrow endothelial cells, both of which are essential for immature and mature B cell retention in the bone marrow. These results suggest that bone marrow endothelial cells can sense and rapidly respond to erythropoietin increase during anemia, thereby regulating B cell emigration from the bone marrow during emergency hematopoiesis.

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Section: Hemorrhagic and Hemolytic Anemia Induce Rapid Release Of Devmentioning

confidence: 99%

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Ito

Hamazaki

Takaori‐Kondo³

et al. 2017

Cell Struct. Funct.

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“…To explore this possibility, we first examined global expression changes in cell adhesion and homing genes by sorting CD19 + B cells from wild-type and Klf3 null spleens for microarray analysis. We found significant changes in a number of key genes, including those with roles in egress from lymphoid organs (CD69 and S1pr3) (25,26) and endothelial cell interaction (CD62L) (Supplemental Table I). …”

Section: Klf3 Is Required For Mz B Cell Positioning In the Spleenmentioning

confidence: 99%

Impaired B Cell Development in the Absence of Krüppel-like Factor 3

Vũ

Gatto

Turner

et al. 2011

The Journal of Immunology

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Krüppel-like factor 3 (Klf3) is a member of the Klf family of transcription factors. Klfs are widely expressed and have diverse roles in development and differentiation. In this study, we examine the function of Klf3 in B cell development by studying B lymphopoiesis in a Klf3 knockout mouse model. We show that B cell differentiation is significantly impaired in the bone marrow, spleen, and peritoneal cavity of Klf3 null mice and confirm that the defects are cell autonomous. In the bone marrow, there is a reduction in immature B cells, whereas recirculating mature cells are noticeably increased. Immunohistology of the spleen reveals a poorly structured marginal zone (MZ) that may in part be caused by deregulation of adhesion molecules on MZ B cells. In the peritoneal cavity, there are significant defects in B1 B cell development. We also report that the loss of Klf3 in MZ B cells is associated with reduced BCR signaling strength and an impaired ability to respond to LPS stimulation. Finally, we show increased expression of a number of Klf genes in Klf3 null B cells, suggesting that a Klf regulatory network may exist in B cells.

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“…Ki67 (Abcam), DAPI (Beyotime), 7-aminoactinomycin D (BD Bioscience), and peanut lectin (PNA)-FITC (SigmaAldrich) were also purchased. Single-cell bone marrow or spleen cell suspensions were prepared and stained (27) for analysis and sorting using a FACSAria II flow cytometer (BD Biosciences). Further analysis was conducted with FlowJo software (TreeStar) for gating or Modifit software (Verity) for cell cycle analysis.…”

Section: Flow Cytometrymentioning

confidence: 99%

Histone Arginine Methylation by PRMT7 Controls Germinal Center Formation via Regulating Bcl6 Transcription

Ying

Mei

Zhang

et al. 2015

The Journal of Immunology

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B cells are the center of humoral immunity and produce Abs to protect against foreign Ags. B cell defects lead to diseases such as leukemia and lymphomas. Histone arginine methylation is important for regulating gene activation and silencing in cells. Although the process commonly exists in mammalian cells, its roles in B cells are unknown. To explore the effects of aberrant histone arginine methylation on B cells, we generated mice with a B cell–specific knockout of PRMT7, a member of the methyltransferases that mediate arginine methylation of histones. In this article, we showed that the loss of PRMT7 led to decreased mature marginal zone B cells and increased follicular B cells and promoted germinal center formation after immunization. Furthermore, mice lacking PRMT7 expression in B cells secreted low levels of IgG1 and IgA. Abnormal expression of germinal center genes (i.e., Bcl6, Prdm1, and Irf4) was detected in conditional knockout mice. By overexpressing PRMT7 in the Raji and A20 cell lines derived from B cell lymphomas, we validated the fact that PRMT7 negatively regulated Bcl6 expression. Using chromatin immunoprecipitation–PCR, we found that PRMT7 could recruit H4R3me1 and symmetric H4R3me2 to the Bcl6 promoter. These results provide evidence for the important roles played by PRMT7 in germinal center formation.

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S1P1 receptor directs the release of immature B cells from bone marrow into blood

Cited by 153 publications

References 60 publications

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Bone Marrow Endothelial Cells Induce Immature and Mature B Cell Egress in Response to Erythropoietin

Impaired B Cell Development in the Absence of Krüppel-like Factor 3

Histone Arginine Methylation by PRMT7 Controls Germinal Center Formation via Regulating Bcl6 Transcription

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