scholarly journals The macrophage-expressed gene (mpeg) 1 identifies a subpopulation of B cells in the adult zebrafish

2019 ◽  
Author(s):  
Giuliano Ferrero ◽  
Etienne Gomez ◽  
Sowmya Iyer ◽  
Mireia Rovira ◽  
Magali Miserocchi ◽  
...  
Keyword(s):  
B Cells ◽  
B Lymphocytes ◽  
The Body ◽  
Mononuclear Phagocytes ◽  
Lymphoid Cells ◽  
Adult Zebrafish ◽  
Specific Expression ◽  
Specific Expression Pattern ◽  
Conserved Gene

ABSTRACTThe mononuclear phagocytic system (MPS) consists of many cells, in particular macrophages, scattered throughout the body. However, there is increasing evidence for the heterogeneity of tissue-resident macrophages, leading to a pressing need for new tools to discriminate MPS subsets from other hematopoietic lineages. Mpeg1.1 is an evolutionary conserved gene encoding perforin-2, a pore-forming protein associated with host defense against pathogens. Zebrafish mpeg1.1:GFP and mpeg1.1:mCherry reporters were originally established to specifically label macrophages. Since, more than 100 peer-reviewed publications have made use of mpeg1.1-driven transgenics for in vivo studies, providing new insights into key aspects of macrophage ontogeny, activation and function. However, while the macrophage-specific expression pattern of the mpeg1.1 promoter has been firmly established in the zebrafish embryo, it is currently not known whether this specificity is maintained through adulthood. Here we report direct evidence that beside macrophages, a subpopulation of B-lymphocytes is marked by mpeg1.1 reporters in most adult zebrafish organs. These mpeg1.1+ lymphoid cells endogenously express mpeg1.1 and can be separated from mpeg1.1+ macrophages by virtue of their light-scatter characteristics using FACS. Remarkably, our analyses also revealed that B-lymphocytes, rather than mononuclear phagocytes, constitute the main mpeg1.1-positive population in irf8null myeloid-defective mutants, which were previously reported to recover tissue-resident macrophages in adulthood. One notable exception are skin macrophages, whose development and maintenance appear to be independent from irf8, similar to mammals. Collectively, our findings demonstrate that irf8 functions in myelopoiesis are evolutionary conserved and highlight the need for alternative macrophage-specific markers to study the MPS in adult zebrafish.SUMMARY SENTENCEMpeg1 is not a restricted macrophage marker, but also labels B cells in the adult zebrafish. Therefore, previously identified irf8-independent macrophages likely consist of B lymphocytes.Graphical Abstract

scholarly journals A RECEPTOR FOR ANTIBODY ON B LYMPHOCYTES

1972 ◽  
Vol 135 (3) ◽  
pp. 610-626 ◽  
Author(s):  
A. Basten ◽  
J. F. A. P. Miller ◽  
J. Sprent ◽  
J. Pye
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Lymphocytes ◽  
Antibody Binding ◽  
Lymphoid Cells ◽  
Secondary Response ◽  
Target Cells ◽  
Binding Studies ◽  
Cell Content

Evidence is presented for the existence on all B lymphocytes, but not on T lymphocytes, of a membrane-associated receptor for antibody. The receptor was detected by a radioautographic technique in which lymphoid cells were incubated with antibody followed by the corresponding radioiodinated antigen. The ease with which antibody eluted during washing indicated that the bond between antibody and cell was weak. The formation of an antibody-antigen complex on the cell surface, however, stabilized the bond and permitted accurate quantitation of cells with adherent antibody. The ability of several combinations of antibody and antigen to adhere to the cells demonstrated the nonspecificity of the phenomenon and emphasized the need for care in interpretation of antigen-binding studies particularly when immune cells are being used. The identity of antibody-binding lymphocytes was established by two different approaches. In the first, mouse lymphocyte populations greatly enriched for either T cells or B cells were examined. Their T cell content was assessed by means of well-established markers such as the θ C3H isoantigen. When this was compared with the number of antibody-binding cells, an inverse relationship was obtained in each instance; thus almost all thoracic duct cells from athymic mice labeled with an immune complex although none were θ positive. The striking reduction in antibody-binding cells observed in bursectomized chickens provided a second and independent line of evidence suggesting that B cells, not T cells, bind antibody. The ability of B cells from primed animals to bind antibody in vivo made it important to test whether this phenomenon was related to the carriage of immunological memory. No correlation was, however, found between membrane-bound antibody and memory. It was proposed that the existence of a receptor of this kind may provide a rational explanation for antibody-dependent killing of target cells and may prove of importance in antigen concentration particularly during the secondary response.

scholarly journals AMPK and the Need to Breathe and Feed: What’s the Matter with Oxygen?

2020 ◽  
Vol 21 (10) ◽  
pp. 3518 ◽  
Author(s):  
A. Mark Evans ◽  
D. Grahame Hardie
Keyword(s):  
Food Choice ◽  
Oxygen Supply ◽  
The Body ◽  
Specific Expression ◽  
Subunit Isoforms ◽  
Specific Expression Pattern ◽  
Available Information ◽  
Amp Activated Protein Kinase ◽  
Do So

We live and to do so we must breathe and eat, so are we a combination of what we eat and breathe? Here, we will consider this question, and the role in this respect of the AMP-activated protein kinase (AMPK). Emerging evidence suggests that AMPK facilitates central and peripheral reflexes that coordinate breathing and oxygen supply, and contributes to the central regulation of feeding and food choice. We propose, therefore, that oxygen supply to the body is aligned with not only the quantity we eat, but also nutrient-based diet selection, and that the cell-specific expression pattern of AMPK subunit isoforms is critical to appropriate system alignment in this respect. Currently available information on how oxygen supply may be aligned with feeding and food choice, or vice versa, through our motivation to breathe and select particular nutrients is sparse, fragmented and lacks any integrated understanding. By addressing this, we aim to provide the foundations for a clinical perspective that reveals untapped potential, by highlighting how aberrant cell-specific changes in the expression of AMPK subunit isoforms could give rise, in part, to known associations between metabolic disease, such as obesity and type 2 diabetes, sleep-disordered breathing, pulmonary hypertension and acute respiratory distress syndrome.

scholarly journals B lymphocytes express and lose syndecan at specific stages of differentiation.

1989 ◽  
Vol 1 (1) ◽  
pp. 27-35 ◽  
Author(s):  
R D Sanderson ◽  
P Lalor ◽  
M Bernfield
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Plasma Cells ◽  
Receptor Expression ◽  
Cell Stage ◽  
Precursor B Cells

Lymphopoietic cells require interactions with bone marrow stroma for normal maturation and show changes in adhesion to matrix during their differentiation. Syndecan, a heparan sulfate-rich integral membrane proteoglycan, functions as a matrix receptor by binding cells to interstitial collagens, fibronectin, and thrombospondin. Therefore, we asked whether syndecan was present on the surface of lymphopoietic cells. In bone marrow, we find syndecan only on precursor B cells. Expression changes with pre-B cell maturation in the marrow and with B-lymphocyte differentiation to plasma cells in interstitial matrices. Syndecan on B cell precursors is more heterogeneous and slightly larger than on plasma cells. Syndecan 1) is lost immediately before maturation and release of B lymphocytes into the circulation, 2) is absent on circulating and peripheral B lymphocytes, and 3) is reexpressed upon their differentiation into immobilized plasma cells. Thus, syndecan is expressed only when and where B lymphocytes associate with extracellular matrix. These results indicate that B cells differentiating in vivo alter their matrix receptor expression and suggest a role for syndecan in B cell stage-specific adhesion.

Autoantibody Production during Chronic Graft-Versus-Host Disease Does Not Associate with Long-Term Persistence of Host B Cells in Humans

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1180-1180
Author(s):  
Simona Piemontese ◽  
Zulma Magnani ◽  
Jacopo Peccatori ◽  
Claudio Bordignon ◽  
Chiara Bonini ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Graft Versus Host Disease ◽  
Cell Depletion ◽  
B Cell Depletion ◽  
Autoantibody Production ◽  
Graft Versus Host

Abstract Background. Chronic graft-versus-host disease (cGvHD) is a common complication of allogeneic hemopoietic cell transplantation (allo-HCT). The pathogenesis of cGvHD is poorly understood. In cGvHD, the homeostasis of B lymphocytes is perturbed, as demonstrated by the production of autoantibodies. B-cell depletion with monoclonal antibodies (mAb) interferes with autoantibody production and ameliorates signs and symptoms of cGvHD. In mouse models, cGvHD and autoantibodies associate with the long-term persistence of host B cells after allo-HCT (Sylvain Perruche et al., Transplantation 2006). It has been postulated that host B cells may present alloantigens to donor T cells and, in turn, receive help for autoantibody production. This could be crucial to the pathogenesis of cGvHD. Aim. To investigate whether the long-term persistence of host B lymphocytes is associated with cGvHD and autoantibodies in humans. Patients and methods. We recruited 13 consecutive patients with active cGvHD (4 mild, 5 moderate, 4 severe according to NIH classification) with a median time of onset of 6 months (range 3–36) from HLA-identical sibling (9 patients) and HLA-matched unrelated (4) allo-HCT. As controls, we chose 10 patients that underwent HLAidentical sibling (2), HLA-matched unrelated (5) or haploidentical (3) allo-HCT and never experienced cGvHD. In the two groups, we studied: circulating autoantibodies, including anti-nuclear (ANA), anti-DNA, anti-extractable nuclear antigen, anti-beta2 glycoprotein, anti-neutrophil cytoplasm, anti-thyroid, anti-mytocondria antibodies, rheumatoid factor, absolute numbers of T (CD3+, CD4+, CD8+), conventional B (CD19+), B1 (CD5+/CD19+) and NK cells (CD16+/CD56+) in the graft and in the peripheral blood, microchimerism by short-tandem repeats (STR) on B, T and myeloid cells purified by immunomagnetic cell sorting (sensitivity 0,01%). Results. Patients with cGvHD had high-titer circulating ANA (>1:160) more frequently than controls (54% versus 10%, P<0,05). All other autoantibodies were negative. Peripheral T-cell counts were lower in patients with cGvHD than in controls (for CD8+ cells P<0,05). This was not due to a difference in the absolute numbers of T lymphocytes within the graft between the two groups. Peripheral counts of conventional B and B1 cells in patients with cGvHD were similar to controls. Autoantibodies and cGvHD were not associated with the persistence of host B lymphocytes, since the analysis of STR on purified B cells revealed that they were all of donor origin. T and myeloid cells were also of donor origin. Of interest, in univariate analysis, in vivo B-cell depletion with mAb for the prophylaxis against Epstein-Barr virus-related lymphoproliferative disease showed a trend towards a lower risk of cGvHD (P=0,06). Conclusions. This study indicates that autoantibody production during cGvHD does not associate with long-term persistence of host B cells in humans. Moreover, it suggests that the early depletion of donor B lymphocytes in vivo may be effective for GvHD prophylaxis

scholarly journals The De Novo Methyltransferases DNMT3a and DNMT3b Target the Murine Gammaherpesvirus Immediate-Early Gene 50 Promoter during Establishment of Latency

2010 ◽  
Vol 84 (10) ◽  
pp. 4946-4959 ◽  
Author(s):  
Kathleen S. Gray ◽  
J. Craig Forrest ◽  
Samuel H. Speck
Keyword(s):  
Dna Methylation ◽  
B Cells ◽  
B Lymphocytes ◽  
De Novo ◽  
Lytic Replication ◽  
Immediate Early ◽  
Murine Gammaherpesvirus ◽  
Distal Gene

ABSTRACT The role of epigenetic modifications in the regulation of gammaherpesvirus latency has been a subject of active study for more than 20 years. DNA methylation, associated with transcriptional silencing in mammalian genomes, has been shown to be an important mechanism in the transcriptional control of several key gammaherpesvirus genes. In particular, DNA methylation of the functionally conserved immediate-early replication and transcription activator (RTA) has been shown to regulate Epstein-Barr virus and Kaposi's sarcoma-associated herpesvirus Rta expression. Here we demonstrate that the murine gammaherpesvirus (MHV68) homolog, encoded by gene 50, is also subject to direct repression by DNA methylation, both in vitro and in vivo. We observed that the treatment of latently MHV68-infected B-cell lines with a methyltransferase inhibitor induced virus reactivation. In addition, we show that the methylation of the recently characterized distal gene 50 promoter represses activity in a murine macrophage cell line. To evaluate the role of de novo methyltransferases (DNMTs) in the establishment of these methylation marks, we infected mice in which conditional DNMT3a and DNMT3b alleles were selectively deleted in B lymphocytes. DNMT3a/DNMT3b-deficient B cells were phenotypically normal, displaying no obvious compromise in cell surface marker expression or antibody production either in naïve mice or in the context of nonviral and viral immunogens. However, mice lacking functional DNMT3a and DNMT3b in B cells exhibited hallmarks of deregulated MHV68 lytic replication, including increased splenomegaly and the presence of infectious virus in the spleen at day 18 following infection. In addition, total gene 50 transcript levels were elevated in the spleens of these mice at day 18, which correlated with the hypomethylation of the distal gene 50 promoter. However, by day 42 postinfection, aberrant virus replication was resolved, and we observed wild-type frequencies of viral genome-positive splenocytes in mice lacking functional DNMT3a and DNMT3b in B lymphocytes. The latter correlated with increased CpG methylation in the distal gene 50 promoter, which was restored to levels similar to those of littermate controls harboring functional DNMT3a and DNMT3b alleles in B lymphocytes, suggesting the existence of an alternative mechanism for the de novo methylation of the MHV68 genome. Importantly, this DNMT3a/DNMT3b-independent methylation appeared to be targeted specifically to the gene 50 promoter, as we observed that the promoters for MHV68 gene 72 (v-cyclin) and M11 (v-bcl2) remained hypomethylated at day 42 postinfection. Taken together, these data provide the first evidence of the importance of DNA methylation in regulating gammaherpesvirus RTA/gene 50 transcription during virus infection in vivo and provide insight into the hierarchy of host machinery required to establish this modification.

scholarly journals Prolonged survival in vivo of unprimed B cells responsive to a T-independent antigen.

1985 ◽  
Vol 161 (6) ◽  
pp. 1581-1586 ◽  
Author(s):  
Y Ron ◽  
J Sprent
Keyword(s):  
Lymph Node ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Thoracic Duct ◽  
Thoracic Duct Lymph ◽  
Cell Transfer ◽  
Adult Mice ◽  
Duct Lymph

Despite earlier evidence to the contrary, it has recently been claimed that most B lymphocytes, including lymph node (LN) and thoracic duct B cells, are short-lived cells of recent marrow origin. To seek direct information on this question, we transferred unprimed LN or thoracic duct B cells from normal mice to xid mice, i.e., mice unresponsive to the T-independent antigen, trinitrophenyl (TNP)-Ficoll. At varying periods after B cell transfer the recipients were challenged with TNP-Ficoll; anti-TNP plaque-forming cells were assayed in the spleen 6 d later. The results showed that the B cell recipients retained responsiveness to TNP-Ficoll for at least 3 mo after transfer. Responsiveness increased within the first 3 wk but then remained relatively constant. These findings imply that, at least for TNP-Ficoll-reactive cells, B cells residing in LN and thoracic duct lymph are not short-lived cells of recent marrow. Indeed, the data suggest that once the pool of recirculating B cells is fully formed in adult mice, further input of newly formed cells from the marrow into the recirculating pool is very limited.

scholarly journals STIMULATION OF ANTIBODY PRODUCTION TO THE HAPTEN 2,4-DINITROBENZENE BY AFFINITY LABELED MURINE LYMPHOID CELLS

1974 ◽  
Vol 139 (4) ◽  
pp. 943-956 ◽  
Author(s):  
David A. Lawrence ◽  
William O. Weigle
Keyword(s):  
Immune Response ◽  
B Cells ◽  
Lymphoid Cells ◽  
Cellular Interaction ◽  
Cell Populations ◽  
Cell Contact ◽  
Spleen Cells ◽  
Normal Spleen ◽  
Thymus Cells

The ability of meta-nitrobenzenediazonium fluoborate (m-NBDF)-labeled thymus and spleen (S) cells to transfer immunity to 2,4-dinitrophenyl (DNP) into irradiated syngeneic recipients was investigated. There was a significant increase in the number of anti-DNP plaque-forming cells (PFC) when m-NBDF-labeled thymus cells and normal spleen cells, or normal thymus cells and m-NBDF-labeled spleen cells were transferred, but not when both thymus- and S-cell populations were labeled and injected together into irradiated recipients. The ability of these cell populations to cooperate and enhance the in vivo immune response to DNP is discussed. The T cells seem to be actively involved in the development of this response; they participate beyond the mere role of carrying and presenting antigen to the B cells. It is suggested that cell to cell contact between T and B cells may be an important factor in the elicitation of an immune response. In addition, the cellular interaction is affected by irradiating the thymus cell preparation and the initiating interaction required for antibody synthesis probably occurs within 48 h after injecting the cell populations into the syngeneic irradiated recipients.

scholarly journals Mast cells enhance proliferation of B lymphocytes and drive their differentiation toward IgA-secreting plasma cells

Blood ◽  
2010 ◽  
Vol 115 (14) ◽  
pp. 2810-2817 ◽  
Author(s):  
Sonia Merluzzi ◽  
Barbara Frossi ◽  
Giorgia Gri ◽  
Serena Parusso ◽  
Claudio Tripodo ◽  
...  
Keyword(s):  
B Cells ◽  
Mast Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Plasma Cells ◽  
Close Contact ◽  
Spatial Interaction ◽  
Significant Inhibition ◽  
Cell Contact

Abstract The evidence of a tight spatial interaction between mast cells (MCs) and B lymphocytes in secondary lymphoid organs, along with the data regarding the abundance of MCs in several B-cell lymphoproliferative disorders prompted us to investigate whether MCs could affect the proliferation and differentiation of B cells. To this aim, we performed coculture assays using mouse splenic B cells and bone marrow–derived MCs. Both nonsensitized and activated MCs proved able to induce a significant inhibition of cell death and an increase in proliferation of naive B cells. Such proliferation was further enhanced in activated B cells. This effect relied on cell-cell contact and MC-derived interleukin-6 (IL-6). Activated MCs could regulate CD40 surface expression on unstimulated B cells and the interaction between CD40 with CD40 ligand (CD40L) on MCs, together with MC-derived cytokines, was involved in the differentiation of B cells into CD138+ plasma cells and in selective immunoglobulin A (IgA) secretion. These data were corroborated by in vivo evidence of infiltrating MCs in close contact with IgA-expressing plasma cells within inflamed tissues. In conclusion, we reported here a novel role for MCs in sustaining B-cell expansion and driving the development of IgA-oriented humoral immune responses.

scholarly journals Immunoglobulin signal transduction guides the specificity of B cell-T cell interactions and is blocked in tolerant self-reactive B cells.

1994 ◽  
Vol 179 (2) ◽  
pp. 425-438 ◽  
Author(s):  
M P Cooke ◽  
A W Heath ◽  
K M Shokat ◽  
Y Zeng ◽  
F D Finkelman ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Transgenic Mice ◽  
B Lymphocytes ◽  
Molecular Mechanisms ◽  
Interleukin 4 ◽  
Th Cells

The specificity of antibody (Ab) responses depends on focusing helper T (Th) lymphocyte signals to suitable B lymphocytes capable of binding foreign antigens (Ags), and away from nonspecific or self-reactive B cells. To investigate the molecular mechanisms that prevent the activation of self-reactive B lymphocytes, the activation requirements of B cells specific for the Ag hen egg lysozyme (HEL) obtained from immunoglobulin (Ig)-transgenic mice were compared with those of functionally tolerant B cells isolated from Ig-transgenic mice which also express soluble HEL. To eliminate the need for surface (s)Ig-mediated Ag uptake and presentation and allow the effects of sIg signaling to be studied in isolation, we assessed the ability of allogeneic T cells from bm12 strain mice to provide in vivo help to C57BL/6 strain-transgenic B cells. Interestingly, non-tolerant Ig-transgenic B cells required both allogeneic Th cells and binding of soluble HEL for efficient activation and Ab production. By contrast, tolerant self-reactive B cells from Ig/HEL double transgenic mice responded poorly to the same combination of allogeneic T cells and soluble HEL. The tolerant B cells were nevertheless normally responsive to stimulation with interleukin 4 and anti-CD40 Abs in vitro, suggesting that they retained the capacity to respond to mediators of T cell help. However, the tolerant B cells exhibited a proximal block in the sIg signaling pathway which prevented activation of receptor-associated tyrosine kinases in response to the binding of soluble HEL. The functional significance of this sIg signaling defect was confirmed by using a more potent membrane-bound form of HEL capable of triggering sIg signaling in tolerant B cells, which markedly restored their ability to collaborate with allogeneic Th cells and produce Ab. These findings indicate that Ag-specific B cells require two signals for mounting a T cell-dependent Ab response and identify regulation of sIg signaling as a mechanism for controlling self-reactive B cells.

Osteoblasts Support Early B Lymphoiesis as well as Stem Cell Proliferation and Myelopoiesis: Identification of the Mammalian Cellular Analog of the Bursa of Fabricius.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 508-508
Author(s):  
Jiang Zhu ◽  
Yi Zhang ◽  
Nacksung Kim ◽  
Yongwon Choi ◽  
Gerard Joe ◽  
...  
Keyword(s):  
Stem Cell ◽  
B Cells ◽  
B Lymphocytes ◽  
Stromal Cells ◽  
The Self ◽  
Bursa Of Fabricius ◽  
Osteoblastic Cells ◽  
Self Renewal

Abstract The self-renewal, survival and differentiation of hematopoietic stem cells (HSC) are greatly influenced by the activities of neighboring osteoblasts and non-osteogenic bone marrow (BM) stromal cells such as fibroblasts, endothelial cells and adipocytes. Previously, we showed that osteoblasts from human long bones support the in vitro self-renewal as well as myeloid differentiation of human CD34+ cord blood cells. Recently, Li’s and Scadden’s groups provided in vivo evidence indicating a primary role of trabecular osteoblasts as a major component of HSC niche and of stromal osteoblastic cells in facilitating the self-renewal of HSCs. We have now asked whether osteoblasts contribute to early lymphopoiesis as well as myelopoiesis, by measuring the cellular outpout of purified HSCs on isolated osteoblasts alone, or with added non-osteoblast stromal cytokines as well. We prepared mature osteoblasts, as monitored and confirmed by homogeneous OPN and CD61 expression, by pretreating osteoblastic cells isolated from neonatal calvaria of C57BL/6 mice (CD45.2) with 1X10−7 M PTH. Purified OB were then co-cultured for 6 days with Lin− BM cells (CD45.1+) isolated from congenic B6 mice(CD45.1) and labeled with CFSE. Osteoblast coculture stimulated the proliferation of Lin− CD45.1+ BM cells 50-fold during culture, with most cells (87%) remaining tightly adherent to the osteoblast monolayer; no live cells were recovered from Lin− BM cell culture without osteoblasts. In addition to mature granulocytes/monocytes, a substantial amount of CD45.1+B220+ B lymphocytes (about 10% of small size cells gated by forward and side scatter), were detected. In contrast, very few CD45.1+Lin-Sca-1+c-Kit+ (LSK) cells or CD45.1+Lin−Sca-1−c-Kit+ (CMP) cells were detected under these conditions. Most B220+ cells attached to osteoblasts were found to be CD43+CD24+ pre-B cells undergoing division. In contrast to the cells recovered attached to the osteoblasts, the pre-B lymphocytes found in suspension were more mature with phenotype of B220+CD43−CD24+. Prevention of direct contact of Lin− BM cells with osteoblasts by Transwell co-culture abrogated the production of pre-B cells in both adherent and suspension compartments, indicating that physical contact is required for the interaction. Interestingly, when 20ng/ml of SCF, 6ng/ml of IL-3, 10ng/ml of IL-6 and 25ng/ml TPO were added to osteoblast/Lin− cell co-culture, B lymphpoiesis was repressed, while the production of CD45.1+LSK HSCs and CMPs was significantly enhanced. These data demonstrate a direct role of osteoblasts in inducing and supporting the early development of B lymphocytes from HSCs or/and common lymphoid progenitors. Additional cytokines, perhaps provided in specific in vivo niches by non-osteogenic stromal cells, cooperate with the stimulatory signals from osteoblasts to promote the survival and expansion of HSCs. Taken together, these results suggest that osteoblasts may be the mammalian analog of the avian Bursa of Fabricius, and that their local degree of proximity to non-osteogenic stromal cells may define specific microniches for stem cell survival, myelopoiesis and/or B lymphopoiesis.

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