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Journal articles on the topic 'B-Lymphocytes Cell Lineage Granulocytes Myeloid Cells Receptors'

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Published: 4 June 2021

Last updated: 15 February 2022

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1

Wognum, AW, TP Visser, MO de Jong, T. Egeland, and G. Wagemaker. "Differential expression of receptors for interleukin-3 on subsets of CD34-expressing hematopoietic cells of rhesus monkeys." Blood 86, no. 2 (1995): 581–91. http://dx.doi.org/10.1182/blood.v86.2.581.bloodjournal862581.

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The target cell specificity of interleukin-3 (IL-3) was examined by flow cytometric analysis of IL-3 receptor (IL-3R) expression on rhesus monkey bone marrow (BM) cells using biotinylated IL-3. Only 2% to 5% of unfractionated cells stained specifically with the biotinylated IL-3 and most of these cells were present within the CD34+ subset. IL-3Rs were detected on small CD34dull/RhLA-DRbright/CD10+/CD27+/CD2-/++ +CD20- cells, which probably represent B-cell precursors. IL-3R+ CD34- BM cells, which were detected at low frequencies, consisted of small CD20dull/surface-IgM+/RhLA-DR+ cells. These c

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2

Hultquist, Anne, Robert Mansson, Mikael Sigvardsson, et al. "Genetic Evidence of a Novel Blood Differentiation Pathway from Lympho-Myeloid Hematopoietic Stem/Progenitor Cells, Independent of Common Myeloid Progenitors." Blood 104, no. 11 (2004): 1696. http://dx.doi.org/10.1182/blood.v104.11.1696.1696.

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Abstract We have recently identified three novel subsets of multipotent hematopoietic stem/progenitor cells (HSCs) in the Lin−Sca-1+c-Kithi (LSK) compartment of adult murine bone marrow based on differential expression of CD34 and the cytokine tyrosine kinase receptor Flt3. Long-term HSCs (LT-HSCs) lack CD34 and Flt3 expression (LSKCD34-flt3-), whereas short-term HSCs (ST-HSCs) are LSKCD34+flt3−. A third LSK population is characterized by co-expression of CD34 and Flt3 (LSKCD34+flt3+) and possess a combined myeloid (granulocyte and monocyte) and lymphoid (B and T cell) differentiation potentia

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3

Pospisil, Vitek, Emanuel Necas, and Tomas Stopka. "PU.1 Activity Determines Fate of Myeloid Progenitor Cells during Lineage Commitment." Blood 108, no. 11 (2006): 4207. http://dx.doi.org/10.1182/blood.v108.11.4207.4207.

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Abstract Myeloid cell commitment is regulated by factors interacting with chromatin in a progenitor cell entering differentiation. PU.1 is an ETS family transcription factor that has been well characterized in inducing myelopoiesis and blocking erythroid differentiation. Conditionally activated PU.1-Estrogen Receptor transgene in mouse PU.1 knockout-derived hematopoietic progenitors is known to induce macrophage differentiation. We observed that manipulation of PU.1 activity by using different levels of PU.1-ER activator, tamoxifen, was capable of producing major populations of myeloid progeny

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4

Till, KJ, J. Burthem, A. Lopez, and JC Cawley. "Granulocyte-macrophage colony-stimulating factor receptor: stage- specific expression and function on late B cells." Blood 88, no. 2 (1996): 479–86. http://dx.doi.org/10.1182/blood.v88.2.479.bloodjournal882479.

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) receptors (GMR) are expressed on myeloid cells throughout their maturational sequence. During myelopoiesis, GM-CSF induces the proliferation of precursors and has multiple effects on more mature cells; such effects include induction of maturation and priming for subsequent stimulation. GMR is expressed on a range of other cell types including acute leukemic blasts of myeloid and lymphoid lineage, but has been little studied on more mature lymphoid cells. Using sensitive triple-layer immunophenotypic techniques, we show here that both th

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5

Kubagawa, Hiromi, Ching-Cheng Chen, Le Hong Ho, et al. "Biochemical Nature and Cellular Distribution of the Paired Immunoglobulin-like Receptors, PIR-A and PIR-B." Journal of Experimental Medicine 189, no. 2 (1999): 309–18. http://dx.doi.org/10.1084/jem.189.2.309.

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PIR-A and PIR-B, paired immunoglobulin-like receptors encoded, respectively, by multiple Pira genes and a single Pirb gene in mice, are relatives of the human natural killer (NK) and Fc receptors. Monoclonal and polyclonal antibodies produced against a recombinant PIR protein identified cell surface glycoproteins of ∼85 and ∼120 kD on B cells, granulocytes, and macrophages. A disulfide-linked homodimer associated with the cell surface PIR molecules was identified as the Fc receptor common γ (FcRγc) chain. Whereas PIR-B fibroblast transfectants expressed cell surface molecules of ∼120 kD, PIR-A

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6

Dahl, Richard, Sangeeta R. Iyer, and M. Celeste Simon. "E47 Binds to PU.1 Inhibiting Its Ability To Bind DNA and Activate Gene Expression." Blood 104, no. 11 (2004): 1609. http://dx.doi.org/10.1182/blood.v104.11.1609.1609.

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Abstract The transciption factor PU.1 is required for the development of macrophages, granulocytes, and B lymphocytes. Additionally its protein concentration in multipotential hematopoietic progenitor cells regulates cell fate decisions with high levels of PU.1 directing myeloid cell fate acquisition and low levels directing B cell fate acquisition. Potentially high levels of PU.1 are required for myeloid development in order to overcome repressive effects of B cell lineage specific factors. The essential B cell factor BSAP (Pax-5) was shown to associate with PU.1 and repress its transactivati

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7

Veiby, OP, SD Lyman, and SE Jacobsen. "Combined signaling through interleukin-7 receptors and flt3 but not c- kit potently and selectively promotes B-cell commitment and differentiation from uncommitted murine bone marrow progenitor cells." Blood 88, no. 4 (1996): 1256–65. http://dx.doi.org/10.1182/blood.v88.4.1256.bloodjournal8841256.

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Multiple cytokines can synergize to stimulate the in vitro proliferation and exclusive myeloid differentiation of multipotent bone marrow progenitor cells. The ligand for c-kit (stem cell factor [SCF]) plays a key role in stimulating myeloid and erythroid cell production of primitive hematopoietic progenitors. SCF in combination with interleukin-7 (IL-7) can also stimulate the combined myeloid and B-cell differentiation of uncommitted hematopoietic progenitor cells as well as the growth of early B-cell progenitor cells, although the involvement of c-kit in early B lymphopoiesis remains controv

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8

Zhou, Lan, Quanjian Yan, David Yao, Lebing W. Li, Stanton L. Gerson, and John B. Lowe. "Notch-Dependent Control of Blood Lineage Development is Modified by Fucosylation." Blood 112, no. 11 (2008): 2448. http://dx.doi.org/10.1182/blood.v112.11.2448.2448.

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Abstract Notch receptors are conserved cell surface molecules essential for hematopoietic cell fate determination. Activated Notch enhances self-renewal of hematopoietic stem cells and promotes T lymphopoiesis. O-linked fucose moieties attached to the EGF domains of Notch receptors and its modification by Fringe can strongly modulate Notch signaling. Our recently published results indicate that Notch-dependent signaling controls myelopoiesis both in vitro and in vivo, and identify a requirement for Notch fucosylation in the expression of Notch ligand binding activity and Notch signaling effici

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9

Anderlini, Paolo, and Richard E. Champlin. "Biologic and molecular effects of granulocyte colony-stimulating factor in healthy individuals: recent findings and current challenges." Blood 111, no. 4 (2008): 1767–72. http://dx.doi.org/10.1182/blood-2007-07-097543.

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Recombinant human granulocyte colony-stimulating factor (rhG-CSF) is widely used in healthy donors for collection of peripheral blood progenitor cells (PBPCs) for allogeneic transplantation and granulocytes for transfusion. The spectrum of its biologic and molecular activities in healthy individuals is coming into sharper focus, creating a unique set of challenges and clarifying the need to monitor and safeguard donor safety. Accumulating evidence indicates that rhG-CSF effects are not limited to the myeloid cell lineage. This may reflect the presence of functional G-CSF receptors on other cel

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10

Papapetrou, Eirini P., Damian Kovalovsky, Laurent Beloeil, Derek Sant’Angelo, and Michel Sadelain. "microRNA-Mediated Gene Regulation Effectively Restricts In Vivo Transgene Expression in Hematopoietic Stem Cell Progeny." Blood 110, no. 11 (2007): 193. http://dx.doi.org/10.1182/blood.v110.11.193.193.

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Abstract Stem cell engineering and targeted in vivo gene delivery increasingly require tight control of transgene expression. Lineage- and differentiation stage-specific gene regulation is classically afforded by pol-II-dependent transcript regulation. A super-imposed layer of post-transcriptional control would be valuable to correct undesirable expression patterns or fine-tune developmentally regulated or inducible gene expression. microRNAs (miRNAs) have recently emerged as potent repressors of gene expression at the post-transcriptional level. In this study, we investigate the potential of

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11

Hosokawa, Kohei, Sachiko Kajigaya, Keyvan Keyvanfar, et al. "Whole Transcriptome Sequencing Identifies Novel Pathways Associated with Paroxysmal Nocturnal Hemoglobinuria- Increased CXCR2 Expression in PNH Granulocytes." Blood 126, no. 23 (2015): 3608. http://dx.doi.org/10.1182/blood.v126.23.3608.3608.

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Abstract Background. Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder that arises from hematopoietic stem cells (HSCs). PNH is caused by a somatic mutation in the X-linked phosphatidylinositol glycan class A gene (PIG-A), responsible for a deficiency in glycosyl phosphatidylinositol-anchored proteins (GPI-APs). PNH is a clonal disease that originates from HSCs, as the originating PIGA mutation is present in cells of multiple lineages, including myeloid, erythroid, and lymphoid cells. However, a critical question regarding PNH that has yet to be fully explained despite s

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12

Ishikawa, Fumihiko, Tadafumi Iino, Hiroaki Niiro, et al. "Human Conventional and Plasmacytoid Dendritic Cells Can Originate from Both Lymphoid and Myeloid Progenitors in a New Humanized Mouse System." Blood 106, no. 11 (2005): 2273. http://dx.doi.org/10.1182/blood.v106.11.2273.2273.

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Abstract Dendritic cells play a key role in host defense by presenting exogenous antigens to T cells. Two dendritic cell subsets, conventional dendritic cells (cDCs) and plasmacytoid dendritic cells (pDCs), express distinct repertoire of Toll-like-receptors and recognize different antigens. We previously reported that murine cDCs and pDCs differentiate via either the myeloid or the lymphoid pathway (Shigematsu et al. Immunity ). It is, however, still unclear whether human cDCs and pDCs develop from myeloid, lymphoid or both lineages. In order to analyze the in vivo differentiation of human den

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13

Liu, Yi, Carol Swiderski, Barry Grimes, Chi Wang, Ying Liang, and Gary Van Zant. "A Cell-Autonomous Myeloproliferative Phenotype Caused by Loss of Latexin in Stem and Progenitor Cells." Blood 120, no. 21 (2012): 2314. http://dx.doi.org/10.1182/blood.v120.21.2314.2314.

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Abstract Abstract 2314 We have previously shown a novel role for Latexin (Lxn), a carboxypeptidase inhibitor, in influencing the size of murine hematopoietic stem cell (HSC) population. Lxn negatively regulates HSC population size by enhancing apoptosis while repressing proliferation and self-renewal. However, the major mechanisms underlying this phenotype remain unknown. To further study the functionality of latexin in hematopoiesis, we generated a knock-out mouse model (Lxn−/− mouse) with a truncation of Lxn exon 2 to exon 5. Blood cell counts showed that lymphocytes, neutrophils, eosinophil

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14

Iwata, Mineo, Manoj Pillai, H. Joachim Deeg, Ghislain Opdenakker, and Beverly Torok-Storb. "Inducible Levels of Gelatinase B/Matrix Metalloproteinase-9 Gene Expression in Monocytes Are Associated with Marrow Cellularity in Myelodysplastic Syndrome (MDS)." Blood 106, no. 11 (2005): 1391. http://dx.doi.org/10.1182/blood.v106.11.1391.1391.

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Abstract Evidence suggests that within the hematopoietic microenvironment (ME) stromal cell function can be modified by activities produced by monocytes/macrophages and that the reciprocal is also true; stroma can influence monocyte function. Critical regulatory molecules produced by stroma are often membrane bound until cleaved by metalloproteinases (MMP); cleavage can serve to either activate or inactivate their functions, making MMPs critical components of hematopoietic regulation. We report here that gene and protein expression of human matrix metalloproteinase-9 (MMP-9) is induced in mono

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15

Lee, Angel W., Heather Grifka, and Soojie Yu. "Gab2 Is a Key Determinant of Mononuclear Phagocyte Development and a Regulator of Macrophage Recruitment in Acute Inflammation." Blood 112, no. 11 (2008): 3857. http://dx.doi.org/10.1182/blood.v112.11.3857.3857.

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Abstract Colony Stimulating Factor-1 (CSF-1) acts through the CSF-1R to regulate proliferation, survival and differentiation of mononuclear phagocytes (MNPs). GAB2, a scaffolding protein, modulates signals from numerous receptors, through recruitment of phosphatidylinositol 3-kinase (PI3K) and SHP2 phosphatase. Previously we reported at this meeting (Lee et al., Blood110:2197, 2007) that under steady conditions, GAB2−/− mice showed a significant reduction in the number of bone marrow (BM) tissue macrophages (Mφs) and dramatic decreases in the number of CSF-1 dependent colony forming units (CFU

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16

Xie, Stephanie Zhi-Juan, Kerstin Kaufmann, Olga I. Gan, Sasan Zandi, Naoya Takayama, and John E. Dick. "Sphingolipids Regulate Myeloid-Erythroid Fate Determination in Human Hematopoiesis." Blood 128, no. 22 (2016): 3865. http://dx.doi.org/10.1182/blood.v128.22.3865.3865.

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Abstract The established model of hematopoiesis posits mature blood lineages are derived through successive stages of progenitors that become increasingly lineage-restricted. Whereas the master transcriptional regulators of myeloid-erythroid fate specification such a in Pu.1, Gata1 and CEBPalpha are well studied, the signaling networks that link extrinsic niche signals to lineage commitment is ill-defined. Sphingosine-1-phosphate (S1P) is a bioactive lipid produced from sphingolipid metabolism that in mice has been implicated in HSC egress, lymphocyte trafficking and lymphocyte lineage determi

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17

Tsuji, Noriaki, Kohei Hosokawa, Ryota Urushihara, et al. "Epigenetic Loss of the HLA-DR15 Expression on Hematopoietic Stem Progenitor Cells in Patients with Acquired Aplastic Anemia Characterized By Cyclosporine Dependency: A Novel Mechanism Underlying the Immune Escape of Hematopoietic Stem Progenitor Cells." Blood 136, Supplement 1 (2020): 23–24. http://dx.doi.org/10.1182/blood-2020-136893.

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[Background] HLA-DR15 (DR15) has been implicated in the susceptibility to immune-mediated bone marrow (BM) failure, such as acquired aplastic anemia (AA), wherein the hematopoietic function depends on cyclosporine (CsA), paroxysmal nocturnal hemoglobinuria (PNH) with BM failure, and low-risk myelodysplastic syndrome responsive to immunosuppressive therapy. However, how DR15 contributes to the development of such immune-mediated BM failure remains unclear. Although the copy-number neutral loss of heterozygosity in chromosome 6p (6pLOH) of hematopoietic stem progenitor cells (HSPCs) in AA patien

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18

Pospisil, Vit, Juraj Kokavec, Pavel Burda, et al. "PU.1 Dose-Dependently Induces Granulocyte or Macrophage Commitment by Targeting Lineage Restricted Genes and by Regulating Transcription Factors Egr2, Nab2, Cebpa and Gfi1." Blood 110, no. 11 (2007): 661. http://dx.doi.org/10.1182/blood.v110.11.661.661.

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Abstract PU.1 (Sfpi1) is an ets family transcription factor required for the proper generation of both myeloid (macrophages and neutrophils) and lymphoid lineages (B and T lymphocytes)(Scott 1994, McKercher 1996). Graded expression of exogenous PU.1 in murine PU.1-deficient fetal liver hematopoietic progenitors demonstrated that increased levels of PU.1 are required to initiate development of macrophages (DeKoter, 2000). We have studied the effects of graded expression of PU.1 on its occupancy in chromatin and on the development of myeloid cells in vitro. We measured changes in gene expression

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19

Wu, Zhijie, Shouguo Gao, Sachiko Kajigaya, et al. "Single-Cell RNA Sequencing Reveals a Distinct Transcriptome Signature of Hematopoiesis in GATA2 Deficiency." Blood 134, Supplement_1 (2019): 3735. http://dx.doi.org/10.1182/blood-2019-124774.

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Constitutional GATA2 deficiency caused by heterozygous germline GATA2 mutations has a broad spectrum of clinical phenotypes including systemic infections, lymphedema, cytopenias, myelodysplasia, and a high risk of developing myeloid leukemias. GATA2 deficiency is recognized as a major MDS predisposition syndrome, germline GATA2 mutations are found in 7% of primary MDS cases in children and adolescents. Monosomy 7 and trisomy 8 are frequent chromosomal abnormalities in GATA2 deficiency and features of disease prognosis and malignant transformation. GATA2 mutations mostly affect two zinc finger

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20

Ford, AM, LE Healy, CA Bennett, E. Navarro, E. Spooncer, and MF Greaves. "Multilineage phenotypes of interleukin-3-dependent progenitor cells." Blood 79, no. 8 (1992): 1962–71. http://dx.doi.org/10.1182/blood.v79.8.1962.1962.

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Abstract Interleukin-3 (IL-3)-dependent murine FDCP-mix cells have multilineage differentiation capacity; they are nonleukemic, have a normal karyotype, and are nonimmortalized. These cells coexpress on their cell surface the “early” B-lineage marker B220/CD45R and the myeloid marker Mac-1/iC3b receptor (CR3), transcribe germline T-cell receptor gamma genes, and express the macrophage lineage growth factor receptor gene c- fms as a predominant 8.4-kb transcript. They do not detectably express at the stable mRNA or protein level other lymphoid precursor cell genes including CD2, TdT, lambda 5,

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21

Ford, AM, LE Healy, CA Bennett, E. Navarro, E. Spooncer, and MF Greaves. "Multilineage phenotypes of interleukin-3-dependent progenitor cells." Blood 79, no. 8 (1992): 1962–71. http://dx.doi.org/10.1182/blood.v79.8.1962.bloodjournal7981962.

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Interleukin-3 (IL-3)-dependent murine FDCP-mix cells have multilineage differentiation capacity; they are nonleukemic, have a normal karyotype, and are nonimmortalized. These cells coexpress on their cell surface the “early” B-lineage marker B220/CD45R and the myeloid marker Mac-1/iC3b receptor (CR3), transcribe germline T-cell receptor gamma genes, and express the macrophage lineage growth factor receptor gene c- fms as a predominant 8.4-kb transcript. They do not detectably express at the stable mRNA or protein level other lymphoid precursor cell genes including CD2, TdT, lambda 5, and BP1.

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22

Ingley, E., and IG Young. "Characterization of a receptor for interleukin-5 on human eosinophils and the myeloid leukemia line HL-60." Blood 78, no. 2 (1991): 339–44. http://dx.doi.org/10.1182/blood.v78.2.339.339.

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Abstract Interleukin-5 (IL-5) promotes the growth and differentiation of human eosinophils and may regulate the selective eosinophilia and eosinophil activation seen in certain diseases. Radiolabeled recombinant human IL- 5 (hIL-5) was used to characterize the IL-5 receptor present on normal human eosinophils and on the myeloid leukemia line HL-60, which can be induced to differentiate into eosinophilic cells. Binding studies with eosinophils and HL-60 cells grown under alkaline conditions demonstrated similar high-affinity binding sites for hIL-5 on both cell types with kd values of approxima

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23

Ingley, E., and IG Young. "Characterization of a receptor for interleukin-5 on human eosinophils and the myeloid leukemia line HL-60." Blood 78, no. 2 (1991): 339–44. http://dx.doi.org/10.1182/blood.v78.2.339.bloodjournal782339.

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Interleukin-5 (IL-5) promotes the growth and differentiation of human eosinophils and may regulate the selective eosinophilia and eosinophil activation seen in certain diseases. Radiolabeled recombinant human IL- 5 (hIL-5) was used to characterize the IL-5 receptor present on normal human eosinophils and on the myeloid leukemia line HL-60, which can be induced to differentiate into eosinophilic cells. Binding studies with eosinophils and HL-60 cells grown under alkaline conditions demonstrated similar high-affinity binding sites for hIL-5 on both cell types with kd values of approximately 400

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24

Smaldone, Giovanni, Luigi Coppola, Mariarosaria Incoronato, et al. "KCTD15 Protein Expression in Peripheral Blood and Acute Myeloid Leukemia." Diagnostics 10, no. 6 (2020): 371. http://dx.doi.org/10.3390/diagnostics10060371.

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Leukocytes are major cellular components of the inflammatory and immune response systems. After their generation in the bone marrow from hematopoietic stem cells, they maturate as granulocytes (neutrophils, eosinophils, and basophils), monocytes, and lymphocytes. The abnormal accumulation and proliferation of immature blood cells (blasts) lead to severe and widespread diseases such as leukemia. We have recently shown that KCTD15, a member of the potassium channel tetramerization domain containing protein family (KCTD), is remarkably upregulated in leukemic B-cells. Here, we extend our investig

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25

Suh, Hyung-Chan, John Gooya, Katie Renn, Alan Friedman, Peter Johnson та Jonathan Keller. "CCAAT Enhancer Binding Protein-α (C/EBPα) Determines Myeloid Versus Erythroid Cell Fate in Multipotential Progenitors." Blood 104, № 11 (2004): 1603. http://dx.doi.org/10.1182/blood.v104.11.1603.1603.

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Abstract C/EBPα is a bZip transcription factor, which is required for granulocyte development, and loss of C/EBPα function is associated with the development of acute myelogenous leukemia and myelodysplastic syndrome. While the precise mechanisms that regulate cell fate decisions during hematopoietic development are largely unknown, expression of transcription factors (PU.1 and GATA-1) can induce lineage conversion. In this regard, C/EBPα can drive the differentiation of B cells into macrophages, and bi-potential cell lines into granulocytes at the expense of macrophages. C/EBPα can also promo

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26

Wang, Xinping, Edward Scott, Charles L. Sawyers, and Alan D. Friedman. "C/EBP Bypasses Granulocyte Colony-Stimulating Factor Signals to Rapidly Induce PU.1 Gene Expression, Stimulate Granulocytic Differentiation, and Limit Proliferation in 32D cl3 Myeloblasts." Blood 94, no. 2 (1999): 560–71. http://dx.doi.org/10.1182/blood.v94.2.560.

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Abstract Within hematopoiesis, C/EBP is expressed only in myeloid cells, and PU.1 is expressed mainly in myeloid and B-lymphoid cells. C/EBP-deficient mice lack the neutrophil lineage and retain monocytes, whereas PU.1-deficient mice lack monocytes and have severely reduced neutrophils. We expressed a C/EBP-estrogen receptor ligand-binding domain fusion protein, C/EBPWT-ER, in 32D cl3 myeloblasts. 32D cl3 cells proliferate in interleukin-3 (IL-3) and differentiate to neutrophils in granulocyte colony-stimulating factor (G-CSF). In the presence of estradiol, C/EBPWT-ER induced morphologic

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Wang, Xinping, Edward Scott, Charles L. Sawyers, and Alan D. Friedman. "C/EBP Bypasses Granulocyte Colony-Stimulating Factor Signals to Rapidly Induce PU.1 Gene Expression, Stimulate Granulocytic Differentiation, and Limit Proliferation in 32D cl3 Myeloblasts." Blood 94, no. 2 (1999): 560–71. http://dx.doi.org/10.1182/blood.v94.2.560.414k41_560_571.

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Within hematopoiesis, C/EBP is expressed only in myeloid cells, and PU.1 is expressed mainly in myeloid and B-lymphoid cells. C/EBP-deficient mice lack the neutrophil lineage and retain monocytes, whereas PU.1-deficient mice lack monocytes and have severely reduced neutrophils. We expressed a C/EBP-estrogen receptor ligand-binding domain fusion protein, C/EBPWT-ER, in 32D cl3 myeloblasts. 32D cl3 cells proliferate in interleukin-3 (IL-3) and differentiate to neutrophils in granulocyte colony-stimulating factor (G-CSF). In the presence of estradiol, C/EBPWT-ER induced morphologic different

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Ishibashi, Tomohiko, Takafumi Yokota, Yusuke Satoh, et al. "MS4A3 Marks Early Myeloid Differentiation in Human Hematopoiesis." Blood 124, no. 21 (2014): 4319. http://dx.doi.org/10.1182/blood.v124.21.4319.4319.

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Abstract Understanding lineage specific markers contributes to investigation into lineage commitment processes in hematopoiesis. Particularly in the human study, information about hematopoietic lineage divergence is essential to refine hematopoietic lineage tree. Lineage markers are also potentially useful for therapeutic target, such as CD20 in B-cell lymphoma, and CD33 in acute myeloid leukemia. We have recently reported that special AT-rich sequence-binding protein 1 (SATB1), a global chromatin organizer, promotes lymphocyte production from hematopoietic stem cells (HSCs) (Immunity 38;1105,

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29

Jacobsen, Sten Eirik W., Robert Mansson, Anne Hultquist, et al. "Evidence for a Novel Blood Lineage Commitment Pathway from Lympho-Myeloid Hematopoietic Stem Cells." Blood 106, no. 11 (2005): 802. http://dx.doi.org/10.1182/blood.v106.11.802.802.

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Abstract We recently identified a novel Lin−Sca-1+c-kithiCD34+Flt3hi (LSKCD34+Flt3hi) lymphoid-primed multipotent progenitor (LMPP) in adult mouse bone marrow which, although possessing a combined lymphoid (B and T cell) and myeloid (granulocyte-monocyte; GM) differentiation potential, have little or no ability to adopt erythroid (E) and megakaryocyte (MK) lineage fates (Adolfsson et al, Cell121:295, 2005). The identification of this lineage restricted lymphomyeloid progenitor implicates the existence of alternative roadmaps for lineage commitment of pluripotent hematopoietic stem cells (HSCs)

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30

Fiedler, Katja, Anca Sindrilaru, Grzegorz Terszowski, et al. "Neutrophil development and function critically depend on Bruton tyrosine kinase in a mouse model of X-linked agammaglobulinemia." Blood 117, no. 4 (2011): 1329–39. http://dx.doi.org/10.1182/blood-2010-04-281170.

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Abstract Bruton tyrosine kinase (Btk) is essential for B cell development and function and also appears to be important for myeloid cells. The bone marrow of Btk-deficient mice shows enhanced granulopoiesis compared with that of wild-type mice. In purified granulocyte-monocyte-progenitors (GMP) from Btk-deficient mice, the development of granulocytes is favored at the expense of monocytes. However, Btk-deficient neutrophils are impaired in maturation and function. Using bone marrow chimeras, we show that this defect is cell-intrinsic to neutrophils. In GMP and neutrophils, Btk plays a role in

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31

Anderson, Karen L., Kent A. Smith, Hugh Perkin, et al. "PU.1 and the Granulocyte- and Macrophage Colony-Stimulating Factor Receptors Play Distinct Roles in Late-Stage Myeloid Cell Differentiation." Blood 94, no. 7 (1999): 2310–18. http://dx.doi.org/10.1182/blood.v94.7.2310.419k34_2310_2318.

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PU.1 is a hematopoietic cell–specific ets family transcription factor. Gene disruption of PU.1 results in a cell autonomous defect in hematopoietic progenitor cells that manifests as abnormal myeloid and B-lymphoid development. Of the myeloid lineages, no mature macrophages develop, and the neutrophils that develop are aberrantly and incompletely matured. One of the documented abnormalities of PU.1 null (deficient) hematopoietic cells is a failure to express receptors for granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage (GM)-CSF, and M-CSF. To elucidate the roles of the my

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Bunting, Kevin D., Heath L. Bradley, Teresa S. Hawley, Richard Moriggl, Brian P. Sorrentino, and James N. Ihle. "Reduced lymphomyeloid repopulating activity from adult bone marrow and fetal liver of mice lacking expression of STAT5." Blood 99, no. 2 (2002): 479–87. http://dx.doi.org/10.1182/blood.v99.2.479.

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Abstract Signal transducers and activators of transcription (STATs) are intracellular mediators of cytokine receptor signals. Because many early-acting growth factors have been implicated in STAT5 activation, this study sought to investigate whether STAT5 may be a transcriptional regulator of hematopoietic stem cell (HSC) long-term repopulating activity. To test this possibility, bone marrow (BM) and fetal liver (FL) cells from mice containing homozygous deletions of both STAT5a and STAT5b genes (STAT5ab−/−) were characterized for hematopoietic repopulating activities. BM and FL grafts were ca

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Lin, Kuan-Yin K., Leslie A. Fogel, Stuart M. Chambers, Nathan C. Boles, and Margaret A. Goodell. "Determining the Distinct Roles of Canonical and Non-Canonical Wnt Pathways in HSC." Blood 108, no. 11 (2006): 1357. http://dx.doi.org/10.1182/blood.v108.11.1357.1357.

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Abstract Hematopoietic stem cells (HSC) can generate all hematopoietic cells. HSCs are defined by their pluripotency and their capacity for self-renewal; however, the factors that control these properties are poorly understood. The Wnt signaling pathway has been implicated in HSC self-renewal. It has been shown by Reya et al that the β-catenin-dependent Wnt pathway is involved in this process. Also, Wnt3a, when included in culture medium, has been shown to maintain HSC in their undifferentiated state. However, due to the redundant and interchangeable roles of Wnt molecules, the impacts of Wnt

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Chicha, Laurie, David Jarrossay, and Markus G. Manz. "Clonal Type I Interferon–producing and Dendritic Cell Precursors Are Contained in Both Human Lymphoid and Myeloid Progenitor Populations." Journal of Experimental Medicine 200, no. 11 (2004): 1519–24. http://dx.doi.org/10.1084/jem.20040809.

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Because of different cytokine responsiveness, surface receptor, and transcription factor expression, human CD11c− natural type I interferon–producing cells (IPCs) and CD11c+ dendritic cells were thought to derive through lymphoid and myeloid hematopoietic developmental pathways, respectively. To directly test this hypothesis, we used an in vitro assay allowing simultaneous IPC, dendritic cell, and B cell development and we tested lymphoid and myeloid committed hematopoietic progenitor cells for their developmental capacity. Lymphoid and common myeloid and granulocyte/macrophage progenitors wer

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35

Iwasaki-Arai, Junko, Hiromi Iwasaki, Toshihiro Miyamoto, Sumiko Watanabe, and Koichi Akashi. "Enforced Granulocyte/Macrophage Colony-stimulating Factor Signals Do Not Support Lymphopoiesis, but Instruct Lymphoid to Myelomonocytic Lineage Conversion." Journal of Experimental Medicine 197, no. 10 (2003): 1311–22. http://dx.doi.org/10.1084/jem.20021843.

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We evaluated the effects of ectopic granulocyte/macrophage colony-stimulating factor (GM-CSF) signals on hematopoietic commitment and differentiation. Lineage-restricted progenitors purified from mice with the ubiquitous transgenic human GM-CSF receptor (hGM-CSFR) were used for the analysis. In cultures with hGM-CSF alone, hGM-CSFR–expressing (hGM-CSFR+) granulocyte/monocyte progenitors (GMPs) and megakaryocyte/erythrocyte progenitors (MEPs) exclusively gave rise to granulocyte/monocyte (GM) and megakaryocyte/erythroid (MegE) colonies, respectively, providing formal proof that GM-CSF signals s

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36

Valk, Peter, Sandra Verbakel, Yolanda Vankan, et al. "Anandamide, a Natural Ligand for the Peripheral Cannabinoid Receptor Is a Novel Synergistic Growth Factor for Hematopoietic Cells." Blood 90, no. 4 (1997): 1448–57. http://dx.doi.org/10.1182/blood.v90.4.1448.

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Abstract We recently demonstrated that the gene encoding the peripheral cannabinoid receptor (Cb2) may be a proto-oncogene involved in murine myeloid leukemias. We show here that Cb2 may have a role in hematopoietic development. RNAse protection analysis showed that Cb2 is normally expressed in spleen and thymus. Cb2 mRNA is also expressed in 45 of 51 cell lines of distinct hematopoietic lineages, ie, myeloid, macrophage, mast, B-lymphoid, T-lymphoid, and erythroid cells. The effect of the fatty acid anandamide, an endogenous ligand for cannabinoid receptors, on primary murine marrow cells and

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Valk, Peter, Sandra Verbakel, Yolanda Vankan, et al. "Anandamide, a Natural Ligand for the Peripheral Cannabinoid Receptor Is a Novel Synergistic Growth Factor for Hematopoietic Cells." Blood 90, no. 4 (1997): 1448–57. http://dx.doi.org/10.1182/blood.v90.4.1448.1448_1448_1457.

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We recently demonstrated that the gene encoding the peripheral cannabinoid receptor (Cb2) may be a proto-oncogene involved in murine myeloid leukemias. We show here that Cb2 may have a role in hematopoietic development. RNAse protection analysis showed that Cb2 is normally expressed in spleen and thymus. Cb2 mRNA is also expressed in 45 of 51 cell lines of distinct hematopoietic lineages, ie, myeloid, macrophage, mast, B-lymphoid, T-lymphoid, and erythroid cells. The effect of the fatty acid anandamide, an endogenous ligand for cannabinoid receptors, on primary murine marrow cells and hematopo

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Drach, D., S. Zhao, J. Drach, et al. "Subpopulations of normal peripheral blood and bone marrow cells express a functional multidrug resistant phenotype [see comments]." Blood 80, no. 11 (1992): 2729–34. http://dx.doi.org/10.1182/blood.v80.11.2729.2729.

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Abstract The multidrug-resistance gene, MDR1 is expressed in many normal tissues, but little is known about its expression in normal hematopoietic cells. Using the monoclonal antibody C219 and flow cytometric analysis, P-glycoprotein (P-gp) was found to be expressed in all peripheral blood (PB) subpopulations (CD4, CD8, CD14, CD19, CD56) except granulocytes. To specifically determine MDR1 gene expression, these PB subpopulations were isolated by fluorescence-activated cell sorting (FACS) and analyzed for MDR1 mRNA by polymerase chain reaction (PCR). All subsets were positive by PCR, but only m

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Drach, D., S. Zhao, J. Drach, et al. "Subpopulations of normal peripheral blood and bone marrow cells express a functional multidrug resistant phenotype [see comments]." Blood 80, no. 11 (1992): 2729–34. http://dx.doi.org/10.1182/blood.v80.11.2729.bloodjournal80112729.

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The multidrug-resistance gene, MDR1 is expressed in many normal tissues, but little is known about its expression in normal hematopoietic cells. Using the monoclonal antibody C219 and flow cytometric analysis, P-glycoprotein (P-gp) was found to be expressed in all peripheral blood (PB) subpopulations (CD4, CD8, CD14, CD19, CD56) except granulocytes. To specifically determine MDR1 gene expression, these PB subpopulations were isolated by fluorescence-activated cell sorting (FACS) and analyzed for MDR1 mRNA by polymerase chain reaction (PCR). All subsets were positive by PCR, but only minimal MD

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Harskamp, Jessica C., Esther H. M. van Egmond, Hans L. Vos, et al. "Myeloid Chimerism Reflects Engraftment of Donor Hematopoiesis, Whereas T Cell Chimerism Reflects Survival and Expansion of Donor and Recipient Residual Mature T Cells Early After T Cell Depleted Allogeneic Stem Cell Transplantation." Blood 114, no. 22 (2009): 4475. http://dx.doi.org/10.1182/blood.v114.22.4475.4475.

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Abstract Abstract 4475 Allogeneic stem cell transplantation (alloSCT) is frequently complicated by life-threatening graft versus host disease (GVHD). Previous studies demonstrated that T cell depletion (TCD) of the graft significantly decreases the incidence and severity of GVHD, and is associated with a higher percentage of patients with mixed chimerism (MC). In most studies chimerism analysis is performed on the total bone marrow (BM) leukocyte fraction, and changes in chimerism are related to engraftment. In this study we investigated whether MC in the total BM leukocyte fraction truly refl

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Lucas-Alcaraz, Daniel. "Granulopoiesis in the Control of Hematopoietic Stem Cell Self-Renewal and Niches." Blood 132, Supplement 1 (2018): SCI—21—SCI—21. http://dx.doi.org/10.1182/blood-2018-99-109517.

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Abstract The bone marrow (BM) vasculature is a critical component of the hematopoietic stem cell (HSC) niche. While the mechanisms through which the vasculature regulates HSC are intensively studied little is known about how this vascular niche is regulated and its function in supporting other aspects of hematopoiesis. We have recently shown that, after myeloablation, BM neutrophils are both sufficient and necessary for the regeneration of the vascular niche. This crosstalk is dependent of TNFα secretion by the neutrophil and TNFR1/TNFR2 expression in the stroma (Bowers et al., 2018). We now d

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Stehling-Sun, Sandra, Rebecca Jimenez, Andrew Hu, and Fernando D. Camargo. "Essential Roles for Mef2c in Lymphoid Commitment and B-Cell Function." Blood 110, no. 11 (2007): 377. http://dx.doi.org/10.1182/blood.v110.11.377.377.

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Abstract MEF2 transcription factors are well-established regulators of muscle development. Recently, work in murine models has identified one of these factors, Mef2c, as an important regulator in the pathogenesis and the development of acute myeloid leukemia (AML). However, little is know about the molecular mechanism and physiological role of Mef2c in hematopoiesis. Using conditional gene ablation, we have discovered an unexpected role for MEF2c in hematopoietic stem cells (HSCs), where it is required for pan-lymphoid commitment. Competitive repopulation experiments using Mef2c-null HSCs dele

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43

Neubauer, A., A. Fiebeler, DK Graham, et al. "Expression of axl, a transforming receptor tyrosine kinase, in normal and malignant hematopoiesis." Blood 84, no. 6 (1994): 1931–41. http://dx.doi.org/10.1182/blood.v84.6.1931.1931.

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Abstract We previously reported the cloning, and characterization of a receptor tyrosine kinase, axl, from two patients with chronic myelogenous leukemia. Herein, we describe the expression pattern of axl in normal and malignant hematopoietic tissue axl message is detected in normal human bone marrow but not significantly in normal blood leukocytes. Cell separation experiments showed that axl is expressed in hematopoietic CD34+ progenitor and marrow stromal cells, at low levels in peripheral monocytes, but not in lymphocytes or granulocytes. Consistent with the normal pattern of axl expression

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44

Neubauer, A., A. Fiebeler, DK Graham, et al. "Expression of axl, a transforming receptor tyrosine kinase, in normal and malignant hematopoiesis." Blood 84, no. 6 (1994): 1931–41. http://dx.doi.org/10.1182/blood.v84.6.1931.bloodjournal8461931.

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We previously reported the cloning, and characterization of a receptor tyrosine kinase, axl, from two patients with chronic myelogenous leukemia. Herein, we describe the expression pattern of axl in normal and malignant hematopoietic tissue axl message is detected in normal human bone marrow but not significantly in normal blood leukocytes. Cell separation experiments showed that axl is expressed in hematopoietic CD34+ progenitor and marrow stromal cells, at low levels in peripheral monocytes, but not in lymphocytes or granulocytes. Consistent with the normal pattern of axl expression, axl RNA

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45

Tsai, Emily J., Harry L. Malech, Martha R. Kirby, et al. "Retroviral transduction of IL2RG into CD34+ cells from X-linked severe combined immunodeficiency patients permits human T- and B-cell development in sheep chimeras." Blood 100, no. 1 (2002): 72–79. http://dx.doi.org/10.1182/blood.v100.1.72.

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Abstract X-linked severe combined immunodeficiency (XSCID) is caused by mutations of the common gamma chain of cytokine receptors, γc. Because bone marrow transplantation (BMT) for XSCID does not provide complete immune reconstitution for many patients and because of the natural selective advantage conferred on lymphoid progenitors by the expression of normal γc, XSCID is a good candidate disease for therapeutic retroviral gene transfer to hematopoietic stem cells. We studied XSCID patients who have persistent defects in B-cell and/or combined B- and T-cell function despite having received T c

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Hunt, Aubrey A., Melissa Ann Steapleton, Isabel Moreno, and Scott Hiebert. "Myeloid Translocation Gene 16 (MTG16) Regulates Lymphopoiesis." Blood 112, no. 11 (2008): 2466. http://dx.doi.org/10.1182/blood.v112.11.2466.2466.

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Abstract The Myeloid Translocation Gene (MTG) family was first discovered through the (8;21) translocation that leads to acute myeloid leukemia. This translocation fuses nearly all of Myeloid Translocation Gene 8 (MTG8) to an N-terminal portion of Acute Myeloid Leukemia 1 (AML1), thus disrupting the normal function of MTG8 as a transcriptional co-repressor. Two other family members have since been identified: Myeloid Translocation Gene 16 (MTG16) and Myeloid Tumor Gene Related-1 (MTGR1), both of which are implicated in leukemogenesis. To examine the physiological roles of Mtg16, a target of th

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Kuwata, Takeshi, I.-Ming Wang, Tomohiko Tamura, et al. "Vitamin A deficiency in mice causes a systemic expansion of myeloid cells." Blood 95, no. 11 (2000): 3349–56. http://dx.doi.org/10.1182/blood.v95.11.3349.

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Abstract To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoi

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48

Kuwata, Takeshi, I.-Ming Wang, Tomohiko Tamura, et al. "Vitamin A deficiency in mice causes a systemic expansion of myeloid cells." Blood 95, no. 11 (2000): 3349–56. http://dx.doi.org/10.1182/blood.v95.11.3349.011k46_3349_3356.

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To examine the role of retinoids in hematopoietic cell growth in vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient mice exhibited a dramatic increase in myeloid cells in bone marrow, spleen, and peripheral blood. The abnormal expansion of myeloid cells was detected from an early stage of vitamin A deficiency and contrasted with essentially normal profiles of T and B lymphocytes. This abnormality was reversed on addition of retinoic acid to the vitamin A–deficient diet, indicating that the myeloid cell expansion is a direct result of retinoic acid de

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49

Stewart-Akers, AM, JS Cairns, DJ Tweardy, and SA McCarthy. "Granulocyte-macrophage colony-stimulating factor augmentation of T-cell receptor-dependent and T-cell receptor-independent thymocyte proliferation." Blood 83, no. 3 (1994): 713–23. http://dx.doi.org/10.1182/blood.v83.3.713.713.

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Abstract The effects of granulocyte-macrophage colony-stimulating factor (GM- CSF) are not confined to cells of the myeloid lineage. GM-CSF has been shown to have effects on mature T cells and both mature and immature T- cell lines. We therefore examined the GM-CSF responsiveness of murine thymocytes to investigate whether GM-CSF also affected normal immature T lymphocytes. The studies presented here indicate that GM-CSF augments accessory cell (AC)-dependent T-cell receptor (TCR)-mediated proliferation of unseparated thymocyte populations. To identify the GM- CSF responsive cell type, thymic

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50

Stewart-Akers, AM, JS Cairns, DJ Tweardy, and SA McCarthy. "Granulocyte-macrophage colony-stimulating factor augmentation of T-cell receptor-dependent and T-cell receptor-independent thymocyte proliferation." Blood 83, no. 3 (1994): 713–23. http://dx.doi.org/10.1182/blood.v83.3.713.bloodjournal833713.

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The effects of granulocyte-macrophage colony-stimulating factor (GM- CSF) are not confined to cells of the myeloid lineage. GM-CSF has been shown to have effects on mature T cells and both mature and immature T- cell lines. We therefore examined the GM-CSF responsiveness of murine thymocytes to investigate whether GM-CSF also affected normal immature T lymphocytes. The studies presented here indicate that GM-CSF augments accessory cell (AC)-dependent T-cell receptor (TCR)-mediated proliferation of unseparated thymocyte populations. To identify the GM- CSF responsive cell type, thymic AC and T

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