scholarly journals The human CD34 hematopoietic stem cell antigen promoter and a 3' enhancer direct hematopoietic expression in tissue culture

Blood ◽  
1992 ◽  
Vol 80 (12) ◽  
pp. 3051-3059 ◽  
Author(s):  
TC Burn ◽  
AB Satterthwaite ◽  
DG Tenen
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Tissue Culture ◽  
Stem Cell ◽  
Transcription Factors ◽  
Progenitor Cell ◽  
Hematopoietic Stem ◽  
Culture Cells ◽  
Human Cd34 ◽  
Tissue Culture Cells

Abstract The human CD34 hematopoietic stem cell antigen is a highly glycosylated type 1 membrane protein of unknown function. CD34 is expressed on 1% to 4% of bone marrow cells, including pluripotent stem cells and committed progenitors of each hematopoietic lineage. CD34 has also been shown to be expressed on the small vessel endothelium of a variety of tissues and on a subset of bone marrow stromal cells. We have chosen to use the human CD34 gene as model to examine the transcription factors and cis-elements required for stem cell/progenitor cell-specific gene regulation. We show here that the CD34 gene is transcriptionally regulated in tissue culture cells. Using a luciferase reporter gene, we have isolated and characterized an active CD34 promoter. A CD34- luciferase construct, containing 4.5 kb of 5′ flanking DNA from a CD34 genomic clone, was 30-fold more active in CD34+ tissue culture cells than in HeLa cells. Sequences from the 3′ end of the CD34 gene were shown to have enhancing activity in CD34+ T-lymphoblastic RPMI-8402 cells and not in CD34- U937 cells or in nonhematopoietic HeLa cells. We also show that a cytidine-guanosine island in the 5′ end of the CD34 gene is heavily methylated in two CD34- hematopoietic cell lines and demethylated in two CD34+ cell lines. Analysis of the CD34 promoter should result in the identification of stem cell/progenitor cell- specific transcription factors and should provide a means to direct the expression of heterologous genes in hematopoietic stem cells and progenitors.

scholarly journals The human CD34 hematopoietic stem cell antigen promoter and a 3' enhancer direct hematopoietic expression in tissue culture

Blood ◽  
1992 ◽  
Vol 80 (12) ◽  
pp. 3051-3059 ◽  
Author(s):  
TC Burn ◽  
AB Satterthwaite ◽  
DG Tenen
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Tissue Culture ◽  
Stem Cell ◽  
Transcription Factors ◽  
Progenitor Cell ◽  
Hematopoietic Stem ◽  
Culture Cells ◽  
Human Cd34 ◽  
Tissue Culture Cells

The human CD34 hematopoietic stem cell antigen is a highly glycosylated type 1 membrane protein of unknown function. CD34 is expressed on 1% to 4% of bone marrow cells, including pluripotent stem cells and committed progenitors of each hematopoietic lineage. CD34 has also been shown to be expressed on the small vessel endothelium of a variety of tissues and on a subset of bone marrow stromal cells. We have chosen to use the human CD34 gene as model to examine the transcription factors and cis-elements required for stem cell/progenitor cell-specific gene regulation. We show here that the CD34 gene is transcriptionally regulated in tissue culture cells. Using a luciferase reporter gene, we have isolated and characterized an active CD34 promoter. A CD34- luciferase construct, containing 4.5 kb of 5′ flanking DNA from a CD34 genomic clone, was 30-fold more active in CD34+ tissue culture cells than in HeLa cells. Sequences from the 3′ end of the CD34 gene were shown to have enhancing activity in CD34+ T-lymphoblastic RPMI-8402 cells and not in CD34- U937 cells or in nonhematopoietic HeLa cells. We also show that a cytidine-guanosine island in the 5′ end of the CD34 gene is heavily methylated in two CD34- hematopoietic cell lines and demethylated in two CD34+ cell lines. Analysis of the CD34 promoter should result in the identification of stem cell/progenitor cell- specific transcription factors and should provide a means to direct the expression of heterologous genes in hematopoietic stem cells and progenitors.

Anti-CD117 (c-Kit) Monoclonal Antibodies Deplete Human Hematopoietic Stem Cells and Facilitate Their Replacement in Humanized NOD/SCID/IL2Rγ−/− Mice: A Non-Toxic Conditioning Regimen for Allotransplantation

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4099-4099
Author(s):  
Aaron C. Logan ◽  
Agnieszka Czechowicz ◽  
Benjamin V. Kelley ◽  
Theingi M. Thway ◽  
Ivan Magana ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Stem Cell ◽  
Hematopoietic Stem Cells ◽  
Potential Candidate ◽  
Partial Recovery ◽  
Flt3 Ligand ◽  
Hematopoietic Stem ◽  
Human Cd34

Abstract Abstract 4099 Engraftment of allogeneic hematopoietic stem cells (HSC) requires conditioning to overcome immunologic and anatomic barriers preventing access to the marrow niche. Most patients who undergo allogeneic hematopoietic cell transplantation (allo-HCT) are prepared with cytotoxic chemotherapy and/or radiation to eliminate these barriers, and to facilitate eradication of malignant cells, if present. Many non-malignant conditions, such as primary immunodeficiencies, hemoglobinopathies, and autoimmune diseases may be successfully treated by transplantation of allogeneic HSC, but the toxicity of conventional conditioning regimens is, in many cases, prohibitive. Targeted elimination of barriers to the HSC niche would be a preferable approach. Signaling via the c-Kit receptor (CD117) is critical for the maintenance of pluripotent HSC. Anti-CD117 monoclonal antibodies (mAbs) deplete HSC and facilitate engraftment of donor HSC in a mouse model of severe combined immunodeficiency (SCID) (Czechowicz et al., Science, 2007). Patients with SCID are highly susceptible to infections, but also have limited immunologic barriers to alloengraftment, making this patient population ideal for studying targeted stem cell depletion to facilitate allo-HSC engraftment. We identified a clinical grade humanized anti-human CD117 mAb (anti-hCD117) as a potential candidate for this purpose. Anti-hCD117 significantly inhibited mitosis in human cord blood and bone marrow derived HSC (Lin−CD34+CD38−CD90+CD45RA−) in liquid and methylcellulose culture containing Flt3 ligand, stem cell factor (SCF), thrombopoietin (TPO), IL-3, and IL-6. To assess in vivo activity of anti-hCD117, we employed it alone, or in combination with alemtuzumab (anti-CD52), to deplete human stem and differentiated cells from hematopoietically humanized NOD/scid/IL2Rg−/− (HuNSG) mice. Pups were conditioned with 100cGy and then humanized by injection of 2000–4000 human HSC into the facial vein on day p2 or intrahepatically on day p4–5. After permitting hematopoietic stabilization for 4–6 months, we confirmed multi-lineage xenochimerism in the peripheral blood (PB) and bone marrow (BM) prior to mAb treatment. After a single treatment with anti-hCD117, mice were depleted of total human leukocytes a median 60% (35–100%; n=11) in the PB and 100% (84–100%; n=10) in the BM at 6 weeks after treatment, with >80% depletion of human myeloid cells in both compartments. Partial recovery of human chimerism was observed at 16 weeks, consistent with recovery of some LT-HSC after anti-hCD117 therapy. The addition of anti-CD52 facilitated clearance of human lymphoid cells not eradicated by anti-hCD117. Human HSC and progenitor cells (Lin−CD34+CD117+; HS/PC) in the bone marrow decreased from 0.4% (0–1.7%) to 0% (0–0.1%; n=10) 6 weeks after treatment with anti-hCD117. We then modeled a human transplant by treating HuNSG mice with anti-hCD117, anti-CD52, or both, to deplete their primary human graft. After monitoring mAb catabolism by ELISA, mice received a second (non-HLA matched) human CD34+ HS/PC graft modified to express the green fluorescent protein using a lentivector. After overnight prestimulation in XVIVO-15 supplemented with SCF, Flt3 ligand, TPO, and IL-3, human CD34+ HS/PC were exposed for 18 hours to lentivector at 1×108 TU/mL. Cells were washed and 80,000 transduced CD34+ HS/PC were injected IV into untreated and mAb-conditioned HuNSG mice. After 6 weeks, PB was evaluated and demonstrated GFP+hCD45+cells in 3/5 (60%) mice treated with anti-hCD117 + anti-CD52, 0/5 mice treated with either anti-hCD117 or anti-CD52 alone, and 1/5 untreated mice. Anti-hCD117 is a promising reagent for depletion of human HSC and facilitation of allo-HSC engraftment. Although anti-hCD117 alone capably depletes human CD34+CD117+ HS/PC and myeloid chimerism in HuNSG mice, the addition of anti-CD52 facilitates engraftment, possibly by reducing alloreactive rejection by T cells from the primary graft. Additional HuNSG mice are receiving second human transplants following mAb conditioning to further explore the utility of combining anti-hCD117 and anti-CD52 for this purpose. These studies will lead the way to minimally toxic allogeneic HSC transplant regimen, and in a broader view, to the application of targeted biological therapies that deplete endogenous stem cells and facilitate their replacement with allogeneic or gene-corrected stem cells. Disclosures: Thway: Amgen, Inc.: Employment. Magana:Amgen, Inc.: Employment. Weissman:Amgen, Inc.: Equity Ownership.

scholarly journals Stem cells: the new “model organism”

2017 ◽  
Vol 28 (11) ◽  
pp. 1409-1411 ◽  
Author(s):  
David G. Drubin ◽  
Anthony A. Hyman
Keyword(s):  
Stem Cells ◽  
Tissue Culture ◽  
Stem Cell ◽  
Human Tissue ◽  
Cell Biology ◽  
Physiological Function ◽  
Model Organism ◽  
Culture Cells ◽  
Tissue Culture Cells ◽  
Biology Research

Human tissue culture cells have long been a staple of molecular and cell biology research. However, although these cells are derived from humans, they have often lost considerable aspects of natural physiological function. Here we argue that combined advances in genome editing, stem cell production, and organoid derivation from stem cells represent a revolution in cell biology. These advances have important ramifications for the study of basic cell biology mechanisms, as well as for the ways in which discoveries in mechanisms are translated into understanding of disease.

scholarly journals Effects of Irradiation on the Functional Characteristics of Human Bone Marrow Mesenchymal Stromal/Stem Cells

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 1589-1589 ◽  
Author(s):  
Masaki Iwasa ◽  
Yasuo Miura ◽  
Aya Fujishiro ◽  
Akihiro Tamura ◽  
Atsushi Sato ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Hematopoietic Stem Cell Transplantation ◽  
Stem Cell Transplantation ◽  
Hematopoietic Stem ◽  
Human Cd34 ◽  
Dose Dependent ◽  
Stromal Stem Cells ◽  
Number Of Cells

Abstract Total-body irradiation is frequently used as a conditioning treatment for hematopoietic stem cell transplantation. Although previous studies have demonstrated that irradiation induces apoptosis and senescence in hematopoietic stem/progenitor cells (HSPCs), its effect on the functional characteristics of human bone marrow mesenchymal stromal/stem cells (BM-MSCs) is largely unknown. Human BM-MSCs were isolated from BM samples according to our previously published method (Stem Cells 32:2245, 2014). BM samples were purchased from AllCells (Emeryville, CA). For the irradiation experiments, BM-MSCs were g-irradiated (Cesium-137) with various doses ranged from 2 to 12 Gy by a Gammmacell Irradiator (Best Theratronics Ltd, Ontario, Canada). We first examined the expansion of g-irradiated human BM-MSCs. When BM-MSCs (0.5 x 105) were cultured on a 10-cm culture dish in advanced-minimal essential medium (Invitrogen, Carlsbad, CA) supplemented with 5% fetal bovine serum (FBS, Invitrogen), the cells expanded rapidly, reached near confluence within 2 weeks, and the average number of cells on day 7 was 6.4 x 105. On the other hand, the number of BM-MSCs that were g-irradiated at 2 Gy, 4 Gy and 12 Gy on day 7 was low at 0.8 x 105, 0.3 x 105, and 0.2 x 105, respectively. The recovery of cell expansion was irradiation dose-dependent; the average number of cells on day 28 was 8.6 x 105 (2 Gy), 3.7 x 105 (4 Gy) and 0.3 x 105 (12 Gy). Next, hematopoiesis-supportive capabilities of g-irradiated human BM-MSCs were examined. Human CD34 positive HSPCs were co-cultured with g-irradiated BM-MSCs in StemSpan Serum-Free Expansion Medium (STEMCELL Technologies, Vancouver, Canada) supplemented with stem cell factor (SCF), Flt3-ligand (Flt3-L), thrombopoietin (TPO), and interleukin (IL)-3. After 10-day co-culture, the expansion of HSPCs was comparable among BM-MSCs with or without g-irradiation. The number of CD33 positive myeloid progenitor cells in the expanded cells was also comparable among BM-MSCs with or without g-irradiation. However, when human CD34 positive HSPCs were co-cultured with g-irradiated BM-MSCs in the complete medium supplemented with 10 ng/mL SCF and 5 ng/mL FLt3-L for 4 weeks, the generation of CD19 positive cells was impaired. The number of CD19 positive cells, which were generated in co-cultures of CD34 positive HSPCs (0.2 x 104) with BM-MSCs that were not g-irradiated, was 1.4 x 104, whereas those in co-cultures with BM-MSCs that were g-irradiated at 2 Gy, 4 Gy and 12 Gy were 0.09 x 104, 0.04 x 104, 0.05 x 104, respectively. With respect to the expression of B-cell lymphopoiesis-associated humoral factors in BM-MSCs, mRNA expression levels of CXCL12/SDF-1, Flt3-L, SCF and IL-7 were decreased in g-irradiated BM-MSCs. Especially, the expression of Flt3-L in BM-MSCs was reduced soon after irradiation exposure. Finally, we found that the osteogenic, adipogenic and chondrogenic differentiation capability of the g-irradiated BM-MSCs were dysregulated, as assessed by both the expression of lineage-specific molecular markers. In conclusion, g-irradiation compromised expansion, differentiation and B-cell lymphopoiesis-supportive capabilities of human BM-MSCs in a dose-dependent manner. This study could provide new insights into the role of BM-MSCs in the pathogenesis of immunologic and non-immunologic complications after hematopoietic stem cell transplantation. Disclosures No relevant conflicts of interest to declare.

scholarly journals Generation of Dyskeratosis Congenita-like Hematopoietic Stem Cells through the Stable Inhibition of DKC1

2020 ◽  
Author(s):  
Carlos Carrascoso-Rubio ◽  
Hidde A. Zittersteijn ◽  
Laura Pintado-Berninches ◽  
Beatriz Fernández-Varas ◽  
M. Luz Lozano ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Hematopoietic Stem Cell Transplantation ◽  
Stem Cell Transplantation ◽  
Hematopoietic Stem Cells ◽  
Bone Marrow Failure ◽  
Dyskeratosis Congenita ◽  
Hematopoietic Stem ◽  
Human Cd34

Abstract Dyskeratosis congenita is a rare telomere biology disorder, which results in different clinical manifestations, including severe bone marrow failure. To date, the only curative treatment for bone marrow failure in dyskeratosis congenita patients is allogeneic hematopoietic stem cell transplantation. However due to the toxicity associated to allogeneic hematopoietic stem cell transplantation in dyskeratosis congenita, new non-toxic therapies are recommended to improve the life expectancy of these patients. Since bone marrow biopsies are not routinely performed during the follow-up of dyskeratosis congenita patients, the availability of dyskeratosis congenita hematopoietic stem cells constitutes a major limitation in the development of new hematopoietic therapies for dyskeratosis congenita. Here we aimed at generating dyskeratosis congenita-like human hematopoietic stem cells in which the efficacy of new therapies could be investigated. X-linked dyskeratosis congenita is one of the most frequent variants of dyskeratosis congenita and is associated with an impaired expression of the DKC1 gene. In this study we thus generated dyskeratosis congenita-like hematopoietic stem cells based on the stable knock-down of DKC1 in human CD34+ cells, using lentiviral vectors encoding for DKC1 short hairpin RNAs. At a molecular level, DKC1-interfered CD34+ cells showed a decreased expression of TERC, as well as a diminished telomerase activity and increased DNA damage. Moreover, DKC1-interfered human CD34+ cells showed defective clonogenic ability and were incapable of repopulating the hematopoiesis of immunodeficient NSG mice. The development of dyskeratosis congenita-like hematopoietic stem cells will facilitate the understanding of the molecular and cellular basis of the bone marrow failure characteristic of dyskeratosis congenita patients, and will serve as a platform for the development of new hematopoietic therapies for dyskeratosis congenita patients.

Abstract 13: Plasminogen Is Required for Hematopoietic Stem Cell-Mediated Cardiac Repair After Myocardial Infarction

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Yanqing Gong ◽  
Jane Hoover-Plow ◽  
Ying Li
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Tissue Repair ◽  
Critical Role ◽  
Cardiac Repair ◽  
Internal Diameter ◽  
Hematopoietic Stem

Ischemic heart disease, including myocardial infarction (MI), is the primary cause of death throughout the US. Granulocyte colony-stimulating factor (G-CSF) is used to mobilize hematopoietic progenitor and stem cells (HPSC) to improve cardiac recovery after MI. However, poor-mobilization to G-CSF is observed in 25% of patients and 10-20% of healthy donors. Therefore, a better understanding of the underlying mechanisms regulating G-CSF-induced cardiac repair may offer novel approaches for strengthening stem cell-mediated therapeutics. Our previous studies have identified an essential role of Plg in HPSC mobilization from bone marrow (BM) in response to G-CSF. Here, we investigate the role of Plg in G-CSF-stimulated cardiac repair after MI. Our data show that G-CSF significantly improves cardiac tissue repair including increasing neovascularization in the infarct area, and improving ejection fraction and LV internal diameter by echocardiogram in wild-type mice. No improvement in tissue repair and heart function by G-CSF is observed in Plg -/- mice, indicating that Plg is required for G-CSF-regulated cardiac repair after MI. To investigate whether Plg regulates HPSC recruitment to ischemia area, bone marrow transplantion (BMT) with EGFP-expressing BM cells was performed to visualize BM-derived stem cells in infarcted tissue. Our data show that G-CSF dramatically increases recruitment of GFP+ cells (by 16 fold) in WT mice but not in Plg -/- mice, suggesting that Plg is essential for HPSC recruitment from BM to the lesion sites after MI. In further studies, we investigated the role of Plg in the regulation of SDF-1/CXCR-4 axis, a major regulator for HPSC recruitment. Our results show that G-CSF significantly increases CXCR-4 expression in infarcted area in WT mice. While G-CSF-induced CXCR-4 expression is markedly decreased (80%) in Plg -/- mice, suggesting Plg may regulate CXCR-4 expression during HSPC recruitment to injured heart. Interestingly, Plg does not affect SDF-1 expression in response to G-CSF treatment. Taken together, our findings have identified a critical role of Plg in HSPC recruitment to the lesion site and subsequent tissue repair after MI. Thus, targeting Plg may offer a new therapeutic strategy to improve G-CSF-mediated cardiac repair after MI.

scholarly journals The quiescent fraction of chronic myeloid leukemic stem cells depends on BMPR1B, Stat3 and BMP4-niche signals to persist in patients in remission

Haematologica ◽  
2020 ◽  
Vol 106 (1) ◽  
pp. 111-122 ◽  
Author(s):  
Sandrine Jeanpierre ◽  
Kawtar Arizkane ◽  
Supat Thongjuea ◽  
Elodie Grockowiak ◽  
Kevin Geistlich ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Tyrosine Kinase ◽  
Stromal Cells ◽  
Kinase Inhibitor ◽  
Bmp Signaling ◽  
Myelogenous Leukemia ◽  
Leukemic Stem Cells ◽  
Hematopoietic Stem

Chronic myelogenous leukemia arises from the transformation of hematopoietic stem cells by the BCR-ABL oncogene. Though transformed cells are predominantly BCR-ABL-dependent and sensitive to tyrosine kinase inhibitor treatment, some BMPR1B+ leukemic stem cells are treatment-insensitive and rely, among others, on the bone morphogenetic protein (BMP) pathway for their survival via a BMP4 autocrine loop. Here, we further studied the involvement of BMP signaling in favoring residual leukemic stem cell persistence in the bone marrow of patients having achieved remission under treatment. We demonstrate by single-cell RNA-Seq analysis that a sub-fraction of surviving BMPR1B+ leukemic stem cells are co-enriched in BMP signaling, quiescence and stem cell signatures, without modulation of the canonical BMP target genes, but enrichment in actors of the Jak2/Stat3 signaling pathway. Indeed, based on a new model of persisting CD34+CD38- leukemic stem cells, we show that BMPR1B+ cells display co-activated Smad1/5/8 and Stat3 pathways. Interestingly, we reveal that only the BMPR1B+ cells adhering to stromal cells display a quiescent status. Surprisingly, this quiescence is induced by treatment, while non-adherent BMPR1B+ cells treated with tyrosine kinase inhibitors continued to proliferate. The subsequent targeting of BMPR1B and Jak2 pathways decreased quiescent leukemic stem cells by promoting their cell cycle re-entry and differentiation. Moreover, while Jak2-inhibitors alone increased BMP4 production by mesenchymal cells, the addition of the newly described BMPR1B inhibitor (E6201) impaired BMP4-mediated production by stromal cells. Altogether, our data demonstrate that targeting both BMPR1B and Jak2/Stat3 efficiently impacts persisting and dormant leukemic stem cells hidden in their bone marrow microenvironment.

Isolation and characterization of human CD34−Lin− and CD34+Lin− hematopoietic stem cells using cell surface markers AC133 and CD7

Blood ◽  
2000 ◽  
Vol 95 (9) ◽  
pp. 2813-2820 ◽  
Author(s):  
Lisa Gallacher ◽  
Barbara Murdoch ◽  
Dongmei M. Wu ◽  
Francis N. Karanu ◽  
Mike Keeney ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Surface Markers ◽  
Cell Surface Markers ◽  
Hematopoietic Stem ◽  
Human Cd34 ◽  
Cd34 Cells

Recent evidence indicates that human hematopoietic stem cell properties can be found among cells lacking CD34 and lineage commitment markers (CD34−Lin−). A major barrier in the further characterization of human CD34− stem cells is the inability to detect this population using in vitro assays because these cells only demonstrate hematopoietic activity in vivo. Using cell surface markers AC133 and CD7, subfractions were isolated within CD34−CD38−Lin− and CD34+CD38−Lin− cells derived from human cord blood. Although the majority of CD34−CD38−Lin− cells lack AC133 and express CD7, an extremely rare population of AC133+CD7− cells was identified at a frequency of 0.2%. Surprisingly, these AC133+CD7− cells were highly enriched for progenitor activity at a frequency equivalent to purified fractions of CD34+ stem cells, and they were the only subset among the CD34−CD38−Lin− population capable of giving rise to CD34+ cells in defined liquid cultures. Human cells were detected in the bone marrow of non-obese/severe combined immunodeficiency (NOD/SCID) mice 8 weeks after transplantation of ex vivo–cultured AC133+CD7− cells isolated from the CD34−CD38−Lin− population, whereas 400-fold greater numbers of the AC133−CD7− subset had no engraftment ability. These studies provide novel insights into the hierarchical relationship of the human stem cell compartment by identifying a rare population of primitive human CD34− cells that are detectable after transplantation in vivo, enriched for in vitro clonogenic capacity, and capable of differentiation into CD34+ cells.

scholarly journals Self-repopulating recipient bone marrow resident macrophages promote long-term hematopoietic stem cell engraftment

Blood ◽  
2018 ◽  
Vol 132 (7) ◽  
pp. 735-749 ◽  
Author(s):  
Simranpreet Kaur ◽  
Liza J. Raggatt ◽  
Susan M. Millard ◽  
Andy C. Wu ◽  
Lena Batoon ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Hematopoietic Stem ◽  
Cell Engraftment ◽  
Key Points ◽  
Bone Marrow Engraftment

Key Points Recipient macrophages persist in hematopoietic tissues and self-repopulate via in situ proliferation after syngeneic transplantation. Targeted depletion of recipient CD169+ macrophages after transplant impaired long-term bone marrow engraftment of hematopoietic stem cells.

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