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Vermeer, Jenny A. F., Ineke D. C. Jansen, Matangi Marthi, Fraser P. Coxon, Charles E. McKenna, Shuting Sun, Teun J. de Vries, and Vincent Everts. "Jaw bone marrow-derived osteoclast precursors internalize more bisphosphonate than long-bone marrow precursors." Bone 57, no. 1 (November 2013): 242–51. http://dx.doi.org/10.1016/j.bone.2013.08.007.
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Hackett, J., M. Bennett, and V. Kumar. "Origin and differentiation of natural killer cells. I. Characteristics of a transplantable NK cell precursor." Journal of Immunology 134, no. 6 (June 1, 1985): 3731–38. http://dx.doi.org/10.4049/jimmunol.134.6.3731.
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Abstract To study the origin and differentiation of natural killer (NK) cells, we developed an assay for the transplantable precursor of NK(YAC-1) cells present in the bone marrow. Mice were depleted of endogenous NK(YAC-1) cells by injection of anti-asialo GM1 antibody, followed by lethal whole body irradiation. Normal syngeneic bone marrow cells were transplanted into such pretreated mice. Regeneration of NK(YAC-1) activity in the recipient mice was monitored by two different assays: the ability of spleen cells to lyse YAC-1 cells in vitro and the ability to clear i.v. injected, 125IUdR-labeled YAC-1 cells from the lungs. With both assays, a dose-response relationship between the number of bone marrow cells injected and the degree of NK(YAC-1) activity generated could be demonstrated. However, the lung clearance assay appeared superior because the NK regeneration could be detected earlier and with lower numbers of injected marrow cells. With this assay, several characteristics of the NK precursors and their differentiation could be defined. 1) The generation of mature, lytic NK cells from their transplantable precursor requires an intact "marrow microenvironment" in the recipient mice, because differentiation failed to occur in mice rendered osteopetrotic by estradiol treatment. 2) The NK(YAC-1) precursors lack the surface antigens (NK-2.1, asialo GM1, Qa-5, Thy-1) that are characteristically seen on mature NK cells. 3) The NK-precursors could be eliminated from the bone marrow with anti-Qa-2 or anti-H-2 antisera + complement, indicating that these two antigens are expressed on the precursors. The relationship between NK(YAC-1) precursors and multipotent myeloid stem cells (CFU-S) was investigated by utilizing W/Wv and Sl/Sld mutant mice. Bone marrow cells of W/Wv anemic mice, although markedly deficient in CFU-S, have a normal frequency of NK(YAC-1) precursors. Sl/Sld mice that lack a suitable microenvironment for the development of CFU-S allowed normal differentiation of NK(YAC-1) precursors when transplanted with normal bone marrow cells. Together, these data suggest that multipotent myeloid progenitor cells, as defined by the CFU-S assay, and the NK(YAC-1) precursors are not closely related.
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Mori, Shinichiro, Ken Shortman, and Li Wu. "Characterization of thymus-seeding precursor cells from mouse bone marrow." Blood 98, no. 3 (August 1, 2001): 696–704. http://dx.doi.org/10.1182/blood.v98.3.696.
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Abstract The nature of the cells that seed the thymus of an irradiated recipient after intravenous (IV) transfer of bone marrow (BM) cells was investigated using 2 approaches. First, direct entry of a small number of donor BM cells into the thymus was tracked using a Ly-5 marker. Second, secondary IV transfer of the seeded thymus cells into a secondary recipient was used as an assay for precursor activity. A range of cell types was found to enter the recipient thymus initially, including B-lineage cells and myeloid cells, but T precursors were undetectable by flow cytometry over the first few days. Although all cells initially entering the thymus proliferated, no sustained thymus reconstitution was seen until day 4, when recognizable T-lineage precursors began to appear. The secondary transfer assays revealed the presence of lymphoid precursors in the recipient thymus, including T, NKT, NK, and B precursor activity, with a notable early burst of B-lineage generative capacity. There was no evidence of sustained myeloid precursor or multipotent stem cell activity, even though these were seen if BM cells were injected directly into the recipient thymus rather than introduced into the bloodstream. It is concluded that even though many cell types may initially enter an irradiated thymus, the thymus acts as a sieve, allowing lymphoid precursors, but not multipotent stem cells, to seed the environmental niches that permit selected precursor cell development and thymus reconstitution.
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Kruger, M. G., and R. L. Riley. "The age-dependent loss of bone marrow B cell precursors in autoimmune NZ mice results from decreased mitotic activity, but not from inherent stromal cell defects." Journal of Immunology 144, no. 1 (January 1, 1990): 103–10. http://dx.doi.org/10.4049/jimmunol.144.1.103.
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Abstract The formation of B lymphocytes is abnormal in autoimmune NZB and (NZB x NZW)F1 mice. With age, the proportion of sIg- Ly-5(220)+ pre-B cells and less mature B cell progenitors in the bone marrow progressively declines, reaching only approximately one-third of normal levels in 20-wk-old NZ mice. To determine the mechanisms responsible for the deficiency of NZ B lineage precursors, the mitotic activity of sIg- Ly-5(220)+ bone marrow cells in vivo was determined in NZ and conventional inbred mice as a function of age. The proportion of sIg- Ly-5(220)+ B cell precursors in (S + G2/M) stages of the cell cycle steadily decreased with age in NZ autoimmune mice. Furthermore, upon metaphase arrest, the rate of entry of sIg- Ly-5(220)+ bone marrow cells into G2/M also decreased with age in NZ mice. Therefore, the mitotic activity of sIg- Ly-5(220)+ B cell precursors is substantially decreased in NZ mice greater than or equal to 20 wk of age. The capacity of the bone marrow stromal microenvironment of NZ mice to support B lineage precursor growth was tested in two ways: 1) the capacity of preformed NZ bone marrow stroma to support B lineage cell growth in long term bone marrow cell culture under lymphopoietic conditions was assessed and 2) the capacity of NZ bone marrow B lineage precursors to expand in vivo after sublethal (200 rad) whole body irradiation was determined. Stroma derived from adult NZ mice supported the growth and development of B lineage lymphocytes in long term bone marrow cell culture to a greater extent than did age-matched conventional murine stroma. Furthermore, sublethal irradiation of older adult NZ mice resulted in some expansion of bone marrow sIg- Ly-5(220)+ B cell precursors in vivo. Therefore, the deficiency of B cell progenitors in the bone marrow of older NZ autoimmune mice is associated with diminished mitotic activity. However, this does not result from defects in the capacity of NZ bone marrow stroma to permit B lineage cell expansion as determined by both in vitro and in vivo experiments. In the absence of a detectable stromal cell defect, it is possible that an active inhibitory process within the bone marrow influences the mitotic activity of B cell precursors in NZ mice.
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Ryan, D. H., B. L. Nuccie, C. N. Abboud, and J. L. Liesveld. "Maturation-dependent adhesion of human B cell precursors to the bone marrow microenvironment." Journal of Immunology 145, no. 2 (July 15, 1990): 477–84. http://dx.doi.org/10.4049/jimmunol.145.2.477.
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Abstract Murine B cell precursors can be induced to proliferate in culture if allowed to bind to bone marrow derived adherent cells prepared under specific conditions. We studied the binding of human B cell precursor subpopulations to various in vitro microenvironments to determine which conditions may potentially be suitable models for human B precursor differentiation. Using the markers CD10, CD34, and CD20, B lineage populations of increasing maturation were quantitated: CD10+/CD34+, CD10+/CD20-, CD10+/CD20+, and CD10-/CD20+ cells in marrow, and CD10-/CD20+ mature B cells in peripheral blood. The adhesion of subpopulations of blood and marrow-derived light density cells to adherent cell layers or matrix was studied following a 2-h incubation in 24-well plates. The absolute number of bound B lineage cells was determined by cell counts and flow cytometry analysis. The adherence of B lineage cells to passaged human marrow fibroblasts (BM-FB) was highest in the most immature CD10+/CD34+ cells (34.3 +/- 4.2%), decreasing steadily with each stage of maturation to the peripheral blood B cells (11.2 +/- 2.4%). Increased adhesion of CD10+ B cell precursors relative to CD10-/CD20+ marrow B cells was confirmed by adhesion studies using sorted cells. The two most immature B lineage cells (CD10+CD34+ and CD10+/CD20-) showed more adherence to BM-FB than any other cell type tested, except for monocytes. Only B lineage precursor cells, erythroid precursors and CD10-/CD34+ cells showed significantly greater binding to BM-FB than to plastic. B lineage precursors bound equally well to primary and passaged human marrow fibroblasts, but bound significantly less well to passaged human foreskin fibroblasts, primary human marrow stroma, extracellular matrix of marrow fibroblasts, or fibronectin. These results suggest that specific binding to marrow fibroblasts is part of the differentiation program of early B lineage precursors. This binding activity gradually and predictably decreases during B lineage differentiation, in contrast to expression of other binding receptors, such as LFA-1 and CD44, which increase during B lineage maturation.
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Li, Peng, Shobi Venkatachalam, Daniela Ospina Cordona, Lorena Wilson, Tibor Kovacsovics, Karen A. Moser, Rodney R. Miles, David B. Beck, Tracy George, and Srinivas K. Tantravahi. "A clinical, histopathological, and molecular study of two cases of VEXAS syndrome without a definitive myeloid neoplasm." Blood Advances 6, no. 2 (January 13, 2022): 405–9. http://dx.doi.org/10.1182/bloodadvances.2021005243.
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Abstract VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is caused by somatic mutations in UBA1 and is identified by a genotype-driven method. This condition affects unrelated men with adultonset inflammatory syndromes in association with hematologic manifestations of peripheral cytopenia and bone marrow myeloid dysplasia. Although bone marrow vacuolization restricted to myeloid and erythroid precursors has been identified in patients with VEXAS, the detailed clinical and histopathological features of peripheral blood and bone marrows remain unclear. The current case report describes the characteristic hematologic findings in patients with VEXAS, including macrocytic anemia, thrombocytopenia, marked hypercellular bone marrow with granulocytic hyperplasia, megaloblastic changes in erythroid precursors, and the absence of hematogones in addition to prominent vacuoles in myeloid and erythroid precursor cells. Characterizing the clinical and hematologic features helps to raise awareness and improve diagnosis of this novel, rare, but potentially underrecognized disease. Prompt diagnosis expands the general knowledgeable and understanding of this disease, and optimal management may prevent patients from developing complications related to this refractory inflammatory syndrome and improve the overall clinical outcome.
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Schatteman, Gina C., Martine Dunnwald, and Chunhua Jiao. "Biology of bone marrow-derived endothelial cell precursors." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H1—H18. http://dx.doi.org/10.1152/ajpheart.00662.2006.
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Over the past decade, the old idea that the bone marrow contains endothelial cell precursors has become an area of renewed interest. While some still believe that there are no endothelial precursors in the blood, even among those who do, there is no consensus as to what they are or what they do. In this review, we describe the problems in identifying endothelial cells and conclude that expression of endothelial nitric oxide synthase may be the most reliable antigenic indicator of the phenotype. The evidence for two different classes of endothelial precursors is also presented. We suggest that, though there is no single endothelial cell precursor, we may be able to use these phenotypic variations to our advantage in better understanding their biology. We also discuss how a variety of genetic, epigenetic, and methodological differences can account for the seemingly contradictory findings on the physiological relevance of bone marrow-derived precursors in normal vascular maintenance and in response to injury. Data on the impact of tumor type and location on the contribution of bone marrow-derived cells to the tumor vasculature are also presented. These data provide hope that we may ultimately be able to predict those tumors in which bone marrow-derived cells will have a significant contribution and design therapies accordingly. Finally, factors that regulate bone marrow cell recruitment to and function in the endothelium are beginning to be identified, and several of these, including stromal derived factor 1, monocyte chemoattractant factor-1, and vascular endothelial growth factor are discussed.
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Antica, M., L. Wu, K. Shortman, and R. Scollay. "Thymic stem cells in mouse bone marrow." Blood 84, no. 1 (July 1, 1994): 111–17. http://dx.doi.org/10.1182/blood.v84.1.111.111.
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Abstract There is still controversy concerning the nature of the stem cells from bone marrow that colonize the thymus during embryogenesis and continually throughout life. To identify the bone marrow stem cells that home to and populate the thymus, we screened murine bone marrow cells for the presence of a population of surface phenotype similar to the earliest known intrathymic precursor. We have identified a population characterized by expression of an intermediate level of heat stable antigen, a very low level of Thy-1, and high levels of CD44 and class I major histocompatibility complex antigens. It is negative for B- cell, granulocyte, macrophage, and erythrocyte markers (B220, Gr-1, Mac- 1, and TER 119). All these markers are common to the intrathymic precursors and bone marrow stem cells. However, this new bone marrow population is Sca-2+, similar to the intrathymic precursor, which makes a clear distinction from the Sca-2- bone marrow hematopoietic stem cells previously characterized. The frequency of the new population in the normal mouse bone marrow is about 0.25%. When transferred intrathymically or intravenously to lethally irradiated mice, it has a higher expansion potential (2 x 10(5)) than has been found for the intrathymic precursors (10(3)), but less than was found for the Sca-2- multipotent stem cell (10(7)). These transfer studies also showed that it was pluripotent, in that its precursor activity was not restricted to the production of T or B lymphocytes. However, it gave a reduced spleen colony number and smaller colonies (day-12 colony-forming unit spleen) when compared with multipotent stem cells. Thus, the cell we have identified appears to be the latest pluripotent cells so far identified in bone marrow and is therefore a good candidate for a bone marrow prothymocyte, but it appears not to be T-cell-committed.
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Antica, M., L. Wu, K. Shortman, and R. Scollay. "Thymic stem cells in mouse bone marrow." Blood 84, no. 1 (July 1, 1994): 111–17. http://dx.doi.org/10.1182/blood.v84.1.111.bloodjournal841111.
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There is still controversy concerning the nature of the stem cells from bone marrow that colonize the thymus during embryogenesis and continually throughout life. To identify the bone marrow stem cells that home to and populate the thymus, we screened murine bone marrow cells for the presence of a population of surface phenotype similar to the earliest known intrathymic precursor. We have identified a population characterized by expression of an intermediate level of heat stable antigen, a very low level of Thy-1, and high levels of CD44 and class I major histocompatibility complex antigens. It is negative for B- cell, granulocyte, macrophage, and erythrocyte markers (B220, Gr-1, Mac- 1, and TER 119). All these markers are common to the intrathymic precursors and bone marrow stem cells. However, this new bone marrow population is Sca-2+, similar to the intrathymic precursor, which makes a clear distinction from the Sca-2- bone marrow hematopoietic stem cells previously characterized. The frequency of the new population in the normal mouse bone marrow is about 0.25%. When transferred intrathymically or intravenously to lethally irradiated mice, it has a higher expansion potential (2 x 10(5)) than has been found for the intrathymic precursors (10(3)), but less than was found for the Sca-2- multipotent stem cell (10(7)). These transfer studies also showed that it was pluripotent, in that its precursor activity was not restricted to the production of T or B lymphocytes. However, it gave a reduced spleen colony number and smaller colonies (day-12 colony-forming unit spleen) when compared with multipotent stem cells. Thus, the cell we have identified appears to be the latest pluripotent cells so far identified in bone marrow and is therefore a good candidate for a bone marrow prothymocyte, but it appears not to be T-cell-committed.
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Osnos, Leah, Virginia Sheikh, Jamie Hahn, Ainhoa Perez-Diez, Irini Sereti, and Irina Maric. "Administration of rhIL-7 Is Associated with Increase in Precursor T-Cells in Bone Marrows of Patients with Idiopathic CD4 Lymphocytopenia." Blood 124, no. 21 (December 6, 2014): 2747. http://dx.doi.org/10.1182/blood.v124.21.2747.2747.
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Abstract Introduction Idiopathic CD4+ Lymphocytopenia (ICL) is a rare, likely heterogeneous syndrome characterized by persistent CD4+ lymphopenia (<300/μl) in the absence of HIV infection or other known immunodeficiency. The diverse clinical presentation may include opportunistic infections, malignancies, and autoimmune diseases. Though the etiology of ICL remains unknown, previous studies have suggested decreased production, proliferation, or survival of CD4+ T-cells. There is currently no FDA-approved therapy for ICL. Methods We analyzed bone marrow core biopsies of 12 ICL patients in a phase I/IIA NIH clinical trial designed to evaluate recombinant human Interleukin-7 (rhIL-7) as a potential therapy for ICL . Subjects received 3 injections of rhIL-7 over two 24-week periods. Bone marrow biopsies were performed at week 1 and week 24 to analyze numbers of T-cells and T-cell precursors at baseline and post rhIL-7 therapy. Peripheral blood T-cell counts were assessed in parallel. Double chromogenic immunohistochemical staining using anti-terminal deoxynucleotidyl transferase (TdT) and anti-CD3 antibodies was performed on fixed, paraffin-embedded samples using an automated stainer (Ventana). Single CD3-positive T-cells and double-positive TdT/CD3 precursor T-cells were counted in at least ten consecutive fields under a light microscope and results expressed as mean positive cell number per field before and after treatment with rhIL-7. Similar staining procedure using TdT and CD79a was performed to evaluate precursor B-cells in the same patient cohort. In addition, bone marrow biopsies from 10 healthy control subjects were analyzed in parallel. Results Compared to healthy controls, ICL patients showed no significant differences in the number of bone marrow precursor T-cells (p=0.069) but had lower levels of mature T-cells (p<0.0001) in marrow core biopsies. These data correlated with presence of peripheral blood T-lymphopenias. ICL patients had higher levels of precursor B-cells that were double positive for TdT/CD79a (p=0.016) compared to control marrows, but showed no significant differences in the number of mature B-cells (p=0.059). After treatment with rhIL-7, bone marrow precursor T-cells increased significantly between weeks 1-24 (p=0.016). Mature T-cells also increased significantly (p=0.031). Precursor B-cells and mature B-cells did not change significantly (p=0.313 and 0.375, respectively). During the same time, peripheral blood CD3+ T-cell counts and CD4+ T-cell counts also increased. Conclusion Novel histological technique for double chromogenic staining allows for the visualization of T-cell precursors in bone marrow biopsies. Our study revealed no evidence that lymphopenia in ICL patients is associated with lack of T-cell precursors in bone marrow, suggesting downstream defects in T-cell differentiation, proliferation or survival. Administration of rhIL-7 was associated with an increase in peripheral blood T-cells and increase in bone marrow precursor T-cells, while B-cell lineage cells remained unchanged. Disclosures No relevant conflicts of interest to declare.
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Pello, Oscar M., María del Carmen Moreno-Ortiz, José Miguel Rodríguez-Frade, Laura Martínez-Muñoz, Daniel Lucas, Lucio Gómez, Pilar Lucas, et al. "SOCS up-regulation mobilizes autologous stem cells through CXCR4 blockade." Blood 108, no. 12 (December 1, 2006): 3928–37. http://dx.doi.org/10.1182/blood-2006-02-006353.
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AbstractThe chemokine CXCL12 influences self-renewal and differentiation of hematopoietic stem cell precursors in bone marrow by directing them toward specific stromalcell components. CXCL12 up-regulates members of the SOCS family through JAK/STAT activation, a mechanism that attenuates chemokine responses. SOCS expression may thus modulate retention of hematopoietic precursors (Sca-1+ c-Kit+Lin– cells) in bone marrow. We show that in bovine growth hormone transgenic mice and in growth hormone–treated mice, SOCS up-regulation correlated with a large number of Sca-1+ c-Kit+Lin– cells in blood. Retroviral transduction of SOCSs blocked in vitro migration of Sca-1+c-Kit+Lin– cells, as well as their capacity to reconstitute lethally irradiated mice. Furthermore, in lethally irradiated mice reconstituted with bone marrow infected by a tetracycline-regulated, SOCS-expressing lentiviral vector, doxycycline treatment promoted rapid, extensive precursor mobilization to the periphery. The results indicate that by blocking CXCR4-mediated functions, SOCSs modulate hematopoietic precursor cell retention in bone marrow, and suggest the therapeutic interest of SOCS manipulation in several pathologic situations.
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Butturini, A., and RP Gale. "Long-term bone marrow culture in persons with Fanconi anemia and bone marrow failure." Blood 83, no. 2 (January 15, 1994): 336–39. http://dx.doi.org/10.1182/blood.v83.2.336.336.
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Abstract Fanconi anemia is an autosomal recessive disease characterized by a high risk of developing bone marrow (BM) failure and acute myelogenous leukemia. We studied growth of hematopoietic progenitor cells in long- term BM culture (LTBMC) in 8 persons with Fanconi anemia and BM failure. Although LTBMC were initiated with very few BM cells, an adherent layer formed in cultures from 7 persons. In these cultures, the number of nonadherent cells increased for 10 to 15 days. Cell growth continued until cultures were terminated at day 35 to 40. During the first 2 weeks of culture, most nonadherent cells were differentiated myeloid cells. By days 35 to 40, the adherent layer contained cells able to initiate secondary LTBMCs. These data indicate that hematopoietic precursors cells able to proliferate and differentiate in vitro are present in the BM of persons with Fanconi anemia and BM failure. They suggest that mechanisms other than absent precursor cells are responsible for BM failure in Fanconi anemia.
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Butturini, A., and RP Gale. "Long-term bone marrow culture in persons with Fanconi anemia and bone marrow failure." Blood 83, no. 2 (January 15, 1994): 336–39. http://dx.doi.org/10.1182/blood.v83.2.336.bloodjournal832336.
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Fanconi anemia is an autosomal recessive disease characterized by a high risk of developing bone marrow (BM) failure and acute myelogenous leukemia. We studied growth of hematopoietic progenitor cells in long- term BM culture (LTBMC) in 8 persons with Fanconi anemia and BM failure. Although LTBMC were initiated with very few BM cells, an adherent layer formed in cultures from 7 persons. In these cultures, the number of nonadherent cells increased for 10 to 15 days. Cell growth continued until cultures were terminated at day 35 to 40. During the first 2 weeks of culture, most nonadherent cells were differentiated myeloid cells. By days 35 to 40, the adherent layer contained cells able to initiate secondary LTBMCs. These data indicate that hematopoietic precursors cells able to proliferate and differentiate in vitro are present in the BM of persons with Fanconi anemia and BM failure. They suggest that mechanisms other than absent precursor cells are responsible for BM failure in Fanconi anemia.
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Messner, HA, JE Curtis, MD Minden, D. Tritchler, G. Lockwood, T. Takahashi, J. Lepine, N. Jamal, M. Tweeddale, and U. Wandl. "Clonogenic hemopoietic precursors in bone marrow transplantation." Blood 70, no. 5 (November 1, 1987): 1425–32. http://dx.doi.org/10.1182/blood.v70.5.1425.1425.
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Abstract Multilineage and single-lineage hemopoietic precursors were studied in 102 bone marrow transplant recipients and their respective donors to determine their contribution to clinical outcome as measured by time to engraftment and survival. The patient population was heterogenous with respect to diagnosis and disease status. They included individuals with acute myeloid leukemia (AML), chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL), aplastic anemia, and a few other hematopoietic malignancies. The frequency of various clonogenic precursors in the normal donor population varied considerably. The data yielded a symmetrical distribution. In contrast, most bone marrow transplant recipients presented with significantly reduced numbers of clonogenic cells before transplantation, resulting in skewed distribution profiles. Serial studies of recipients demonstrated a significantly lower than normal level of clonogenic precursors even 3 and 4 years after transplantation. The median values and distribution profiles approximated those observed before transplantation but did not return to measurements obtained for normal donors. Patients with ALL deviated from this pattern. The median values and distribution profiles of clonogenic precursors before transplantation approximated the pattern of normal donors. The frequency of clonogenic progenitors after transplantation, however, remained significantly lower than that of their respective donor or pretransplant values. Cell cycle studies performed after normalization of peripheral blood hematopoietic parameters demonstrated for most recipients that a higher than normal proportion of multipotent cells was in S-phase (P = .011). By univariate and multivariate approaches, clonogenic precursors and clinical parameters were assessed for their contributions to clinical outcome as measured by time to engraftment and survival time. The number of nucleated cells in the transplant inoculum contributed to survival independent of other risk factors. Patients with a higher cell load had a higher probability of surviving than did patients with a lower cell concentration in the transplant inoculum (P = .042). The frequency of clonogenic precursors in the transplant inoculum altered neither survival nor time to engraftment. The time to engraftment was significantly influenced by the frequency of clonogenic megakaryocyte precursors (CFU-M) observed in recipients prior to transplantation (P = .003). Patients with high values engrafted faster than did patients with a low frequency of CFU-M. This was independent of both diagnosis and disease status of the patients at time of transplantation.
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Messner, HA, JE Curtis, MD Minden, D. Tritchler, G. Lockwood, T. Takahashi, J. Lepine, N. Jamal, M. Tweeddale, and U. Wandl. "Clonogenic hemopoietic precursors in bone marrow transplantation." Blood 70, no. 5 (November 1, 1987): 1425–32. http://dx.doi.org/10.1182/blood.v70.5.1425.bloodjournal7051425.
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Multilineage and single-lineage hemopoietic precursors were studied in 102 bone marrow transplant recipients and their respective donors to determine their contribution to clinical outcome as measured by time to engraftment and survival. The patient population was heterogenous with respect to diagnosis and disease status. They included individuals with acute myeloid leukemia (AML), chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL), aplastic anemia, and a few other hematopoietic malignancies. The frequency of various clonogenic precursors in the normal donor population varied considerably. The data yielded a symmetrical distribution. In contrast, most bone marrow transplant recipients presented with significantly reduced numbers of clonogenic cells before transplantation, resulting in skewed distribution profiles. Serial studies of recipients demonstrated a significantly lower than normal level of clonogenic precursors even 3 and 4 years after transplantation. The median values and distribution profiles approximated those observed before transplantation but did not return to measurements obtained for normal donors. Patients with ALL deviated from this pattern. The median values and distribution profiles of clonogenic precursors before transplantation approximated the pattern of normal donors. The frequency of clonogenic progenitors after transplantation, however, remained significantly lower than that of their respective donor or pretransplant values. Cell cycle studies performed after normalization of peripheral blood hematopoietic parameters demonstrated for most recipients that a higher than normal proportion of multipotent cells was in S-phase (P = .011). By univariate and multivariate approaches, clonogenic precursors and clinical parameters were assessed for their contributions to clinical outcome as measured by time to engraftment and survival time. The number of nucleated cells in the transplant inoculum contributed to survival independent of other risk factors. Patients with a higher cell load had a higher probability of surviving than did patients with a lower cell concentration in the transplant inoculum (P = .042). The frequency of clonogenic precursors in the transplant inoculum altered neither survival nor time to engraftment. The time to engraftment was significantly influenced by the frequency of clonogenic megakaryocyte precursors (CFU-M) observed in recipients prior to transplantation (P = .003). Patients with high values engrafted faster than did patients with a low frequency of CFU-M. This was independent of both diagnosis and disease status of the patients at time of transplantation.
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Messner, H. A. "Hemopoietic precursors in human bone marrow transplantation." International Journal of Cell Cloning 4, S1 (1986): 11–18. http://dx.doi.org/10.1002/stem.5530040706.
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YU, Shaohua, cunren Liu, Jianhua Wang, yuelong Liu, liming Zhang, Yingzi Cong, william Grizzle, and huang-Ge Zhang. "Tumor exosomes inhibit differentiation of bone marrow dendritic cells (49.14)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S85. http://dx.doi.org/10.4049/jimmunol.178.supp.49.14.
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Abstract The production of exosomes by tumor cells has been implicated in tumor-associated immune suppression. Here we show that, in mice, exosomes produced by TS/A murine mammary tumor cells target CD11b+Gr-1+ myeloid precursors in the bone marrow in vivo and that this is associated with an accumulation of myeloid precursors in the spleen. Moreover, we demonstrate that TS/A exosomes block differentiation of murine myeloid precursor cells into dendritic cells in vitro. Addition of tumor exosomes at day 0 led to a complete block of differentiation into dendritic cells, whereas addition at later time points was less effective. Similarly, exosomes produced by human breast tumor cells inhibited differentiation of human monocytes in vitro. The levels of IL-6 and phosphorylated Stat3 were elevated 12 h after tumor exosome stimulation of murine myeloid precursors, and tumor exosomes were less effective in inhibiting differentiation of bone marrow cells isolated from IL-6 knockout mice. These data suggest that tumor exosome-mediated induction of IL-6 plays a role in blocking bone marrow dendritic cell differentiation.
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Acs, Geza, and Virginia A. LiVolsi. "Loss of Membrane Expression of E-Cadherin in Leukemic Erythroblasts." Archives of Pathology & Laboratory Medicine 125, no. 2 (February 1, 2001): 198–201. http://dx.doi.org/10.5858/2001-125-0198-lomeoe.
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Abstract Context.—The special societal relationships existing between various cell types in bone marrow suggests that there may be a link between the adhesive characteristics of hematopoietic cells and their maturation. Egress of the developing hematopoietic cells is also a highly regulated process governed by adhesive interactions. In leukemia, immature blasts are not retained within the marrow, suggesting a breakdown of adhesive mechanisms. Recent reports suggest that E-cadherin, an epithelial adhesion molecule, is expressed on erythroid precursors and megakaryocytes, but not on other hematopoietic marrow elements. Objective.—To characterize the expression pattern of E-cadherin in normal and leukemic erythroid precursors by immunohistochemistry in paraffin-embedded tissue and bone marrow aspirate smears. Methods.—Five normal bone marrow specimens from rib resections, 15 trephine bone marrow biopsy specimens, and 6 bone marrow aspirate smears from the iliac crest of patients with no known leukemia were selected. Fourteen bone marrow biopsy specimens from patients with erythroleukemia were also studied. Immunoperoxidase staining of paraffin-embedded tissue and air-dried aspirate smears for E-cadherin (1:200 dilution, HECD-1 clone) was performed using the avidin-biotin peroxidase technique. Results.—In paraffin-embedded bone marrow biopsy and rib specimens and in air-dried bone marrow aspirate smears, strong membrane expression of E-cadherin was seen in the normal erythroid precursors in all cases. In contrast, no membrane expression of E-cadherin was present in any of the bone marrow biopsy specimens from patients with erythroleukemia. Conclusions.—Immunohistochemical detection of membrane expression of E-cadherin may be a useful tool for identification of erythroid precursors. Cells of erythroleukemia lack membrane expression of E-cadherin, in contrast to their normal counterparts. Further studies are needed to define the potential role of E-cadherin in the maturation of erythroid precursors and to ascertain the significance of loss of membrane expression of E-cadherin in erythroleukemia.
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Lu, L., and D. G. Osmond. "Apoptosis during B lymphopoiesis in mouse bone marrow." Journal of Immunology 158, no. 11 (June 1, 1997): 5136–45. http://dx.doi.org/10.4049/jimmunol.158.11.5136.
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Abstract To evaluate the magnitude of cell death and the critical stages at which it occurs during B lymphopoiesis in mouse bone marrow (BM), we have examined the kinetics of apoptosis at defined stages of B cell differentiation. FACS-sorted B220+ BM cells exhibited a low incidence of morphologically apoptotic cells by electron microscopy. In freshly prepared BM suspensions, the incidence of hypodiploid cells detected by multiparameter flow cytometry was greater among large dividing B220+ surface IgM- (sIgM-) precursor B cells and sIgM(low) immature B lymphocytes than among terminal deoxynucleotidyl transferase+ (TdT+) pro-B cells, small nondividing B220+ sIgM- precursors, and surface IgD+ mature B lymphocytes. During short-term culture, apoptotic cells, identified by both DNA content and in situ DNA strand break labeling, increased linearly with time without macrophage ingestion, providing an assay for the rate of entry into apoptosis. B220+ B lineage cells accumulated in apoptosis more rapidly than cells of other lineages. The apoptotic rate was greater among B220+ sIgM- precursor cells than sIgM+ B cells, and was highest among B220+ mu- pro-B cells. Coculture with stromal cells reduced the apoptotic rate of B220+ sIgM- precursors to a greater extent than that of sIgM+ B lymphocytes. The results lead to estimates of the actual number of B lineage cells undergoing apoptosis per unit time in successive differentiation compartments. The findings indicate that, although influenced by local microenvironmental factors, apoptotic cell death occurs most markedly at two developmental stages associated with Ig heavy chain gene rearrangement and Ag receptor expression, respectively.
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D'Amico, Angela, and Li Wu. "The Early Progenitors of Mouse Dendritic Cells and Plasmacytoid Predendritic Cells Are within the Bone Marrow Hemopoietic Precursors Expressing Flt3." Journal of Experimental Medicine 198, no. 2 (July 21, 2003): 293–303. http://dx.doi.org/10.1084/jem.20030107.
Full textAbstract:
Flt3 ligand (Flt3L) is a growth factor for hemopoietic progenitors and can promote the expansion of both conventional dendritic cells (DCs) and plasmacytoid predendritic cells (p-preDCs). The cells responding to Flt3L treatment and the precursors for the DCs and p-preDCs had not been fully characterized. We examined different mouse bone marrow (BM) hemopoietic precursor populations for the surface expression of Flt3 and tested them for early DC and p-preDC precursor activity. Most DC precursor activity, other than that given by multipotent hemopoietic stem cells, was within the downstream precursors expressing Flt3. The majority of mouse BM common lymphoid precursors expressed high levels of Flt3 and these were the most efficient precursors of both DCs and p-preDCs. In contrast, only a small proportion of the common myeloid precursors (CMPs) expressed Flt3, but the precursor activity for both DCs and p-preDCs was within this minor Flt3+ CMP fraction. The granulocyte and macrophage precursors and pro-B cells did not express Flt3 and had no DC or p-preDC precursor activity. These findings demonstrate that the early precursors for all DC subtypes are within the BM Flt3+ precursor populations, regardless of their lymphoid or myeloid lineage orientation.
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Aprikyan, Andrew A. G., W. Conrad Liles, Julie R. Park, Mechthild Jonas, Emil Y. Chi, and David C. Dale. "Myelokathexis, a congenital disorder of severe neutropenia characterized by accelerated apoptosis and defective expression ofbcl-x in neutrophil precursors." Blood 95, no. 1 (January 1, 2000): 320–27. http://dx.doi.org/10.1182/blood.v95.1.320.
Full textAbstract:
Abstract Myelokathexis is a congenital disorder that causes severe chronic leukopenia and neutropenia. Characteristic findings include degenerative changes and hypersegmentation of mature neutrophils and hyperplasia of bone marrow myeloid cells. The associated neutropenia can be partially corrected by treatment with granulocyte colony-stimulating factor (G-CSF) or granulocyte–macrophage colony-stimulating factor (GM-CSF). These features led us to propose that accelerated apoptosis of neutrophil precursors might account for the neutropenic phenotype. Blood and bone marrow aspirates were obtained from 4 patients (2 unrelated families) with myelokathexis before G-CSF therapy and from 2 of the affected persons after G-CSF therapy (1 μg/kg per day subcutaneously for 3 weeks). Bone marrow was fractionated using immunomagnetic bead cell sorting into CD34+, CD33+/CD34−, and CD15+/CD34−/CD33− cell populations. Examination of these cells by flow cytometry and electron microscopy revealed abundant apoptosis in the CD15+ neutrophil precursor population, characterized by enhanced annexin-V binding, extensive membrane blebbing, condensation of heterochromatin, and cell fragmentation. Colony-forming assays demonstrated significant reduction in a proportion of bone marrow myeloid-committed progenitor cells. Immunohistochemical analysis revealed a selective decrease inbcl-x, but not bcl-2, expression in the CD15+/CD34−/CD33− cell population compared with similar subpopulations of control bone marrow-derived myeloid precursors. After G-CSF therapy, apoptotic features of patients' bone marrow cells were substantially reduced, and the absolute neutrophil counts (ANC) and expression ofbcl-x in CD15+/CD34−/CD33−cells increased. The authors concluded that myelokathexis is a disease characterized by the accelerated apoptosis of granulocytes and the depressed expression of bcl-x in bone marrow-derived granulocyte precursor cells. These abnormalities are partially corrected by the in vivo administration of G-CSF. (Blood. 2000;95:320-327)
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Aprikyan, Andrew A. G., W. Conrad Liles, Julie R. Park, Mechthild Jonas, Emil Y. Chi, and David C. Dale. "Myelokathexis, a congenital disorder of severe neutropenia characterized by accelerated apoptosis and defective expression ofbcl-x in neutrophil precursors." Blood 95, no. 1 (January 1, 2000): 320–27. http://dx.doi.org/10.1182/blood.v95.1.320.001k23_320_327.
Full textAbstract:
Myelokathexis is a congenital disorder that causes severe chronic leukopenia and neutropenia. Characteristic findings include degenerative changes and hypersegmentation of mature neutrophils and hyperplasia of bone marrow myeloid cells. The associated neutropenia can be partially corrected by treatment with granulocyte colony-stimulating factor (G-CSF) or granulocyte–macrophage colony-stimulating factor (GM-CSF). These features led us to propose that accelerated apoptosis of neutrophil precursors might account for the neutropenic phenotype. Blood and bone marrow aspirates were obtained from 4 patients (2 unrelated families) with myelokathexis before G-CSF therapy and from 2 of the affected persons after G-CSF therapy (1 μg/kg per day subcutaneously for 3 weeks). Bone marrow was fractionated using immunomagnetic bead cell sorting into CD34+, CD33+/CD34−, and CD15+/CD34−/CD33− cell populations. Examination of these cells by flow cytometry and electron microscopy revealed abundant apoptosis in the CD15+ neutrophil precursor population, characterized by enhanced annexin-V binding, extensive membrane blebbing, condensation of heterochromatin, and cell fragmentation. Colony-forming assays demonstrated significant reduction in a proportion of bone marrow myeloid-committed progenitor cells. Immunohistochemical analysis revealed a selective decrease inbcl-x, but not bcl-2, expression in the CD15+/CD34−/CD33− cell population compared with similar subpopulations of control bone marrow-derived myeloid precursors. After G-CSF therapy, apoptotic features of patients' bone marrow cells were substantially reduced, and the absolute neutrophil counts (ANC) and expression ofbcl-x in CD15+/CD34−/CD33−cells increased. The authors concluded that myelokathexis is a disease characterized by the accelerated apoptosis of granulocytes and the depressed expression of bcl-x in bone marrow-derived granulocyte precursor cells. These abnormalities are partially corrected by the in vivo administration of G-CSF. (Blood. 2000;95:320-327)
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Uckun, FM, S. Haissig, JA Ledbetter, P. Fidler, DE Myers, V. Kuebelbeck, D. Weisdorf, K. Gajl-Peczalska, JH Kersey, and NK Ramsay. "Developmental hierarchy during early human B-cell ontogeny after autologous bone marrow transplantation using autografts depleted of CD19+ B-cell precursors by an anti-CD19 pan-B-cell immunotoxin containing pokeweed antiviral protein." Blood 79, no. 12 (June 15, 1992): 3369–79. http://dx.doi.org/10.1182/blood.v79.12.3369.3369.
Full textAbstract:
Abstract Sequential immunophenotypes of bone marrow (BM) and peripheral blood (PBL) lymphoid cells from 15 B-lineage acute lymphoblastic leukemia (ALL) patients who underwent autologous bone marrow transplantation (BMT) during complete remission were determined by dual-color immunofluorescence and multiparameter flow cytometry. Autografts were depleted of CD19+ B-cell precursors by an immunochemopurging protocol that combines B43-PAP, a potent anti-CD19 immunotoxin, and the cyclophosphamide congener 4-hydroperoxycyclophosphamide (4-HC). A marked interpatient variation was observed in the appearance and expansion of B-cell precursors repopulating the posttransplant marrow. The expression of CD10 and CD19 antigens during early B-cell ontogeny post-BMT preceded the expression of CD20, CD21, CD22, CD40, and sIgM. The surface antigen profiles of the emerging B-cell precursors were similar to those of fetal liver or fetal bone marrow B-cell precursors. Our comparisons of BM and PBL samples from patients in the early post- BMT period demonstrated that (1) PBL initially contains fewer B-lineage cells than does BM, and (2) circulating B-lineage lymphoid cells have a more mature immunophenotype than do BM B-lineage lymphoid cells. Comparison of the surface antigen profiles of day 30 versus day 100 or year 1 BM or PBL lymphoid cells showed an increase in the percentages of CD10+CD22- undifferentiated lymphocyte precursors, as well as CD19+sIgM- B-cell precursors (pre-pre-B), consistent with a time- dependent expansion of these B-cell precursor populations post-BMT. Importantly, the percentages of CD10+CD22+ and CD19+sIgM+ B-cell precursor (pre-B) populations also increased between 30 days and 1 year post-BMT, confirming the ability of emerging immature B-cell precursors to differentiate along the B-precursor pathway. The acquisition and expression of B-lineage differentiation antigens at different stages of the post-BMT B-cell ontogeny support the notion that the expression of these antigens is developmentally programmed. Similar to patients in previous autologous BMT studies, recipients of B-cell precursor- depleted autografts had normal or nearly normal serum immunoglobulin levels, suggesting that the maturing B-cell/plasma cell populations can produce and secrete immunoglobulins. The development of a functional CD19+ B-lineage lymphoid compartment in recipients of autografts which were depleted of CD19+ B-cell precursors corroborates the previously postulated existence of CD19- B-lineage lymphoid progenitor cells.
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Uckun, FM, S. Haissig, JA Ledbetter, P. Fidler, DE Myers, V. Kuebelbeck, D. Weisdorf, K. Gajl-Peczalska, JH Kersey, and NK Ramsay. "Developmental hierarchy during early human B-cell ontogeny after autologous bone marrow transplantation using autografts depleted of CD19+ B-cell precursors by an anti-CD19 pan-B-cell immunotoxin containing pokeweed antiviral protein." Blood 79, no. 12 (June 15, 1992): 3369–79. http://dx.doi.org/10.1182/blood.v79.12.3369.bloodjournal79123369.
Full textAbstract:
Sequential immunophenotypes of bone marrow (BM) and peripheral blood (PBL) lymphoid cells from 15 B-lineage acute lymphoblastic leukemia (ALL) patients who underwent autologous bone marrow transplantation (BMT) during complete remission were determined by dual-color immunofluorescence and multiparameter flow cytometry. Autografts were depleted of CD19+ B-cell precursors by an immunochemopurging protocol that combines B43-PAP, a potent anti-CD19 immunotoxin, and the cyclophosphamide congener 4-hydroperoxycyclophosphamide (4-HC). A marked interpatient variation was observed in the appearance and expansion of B-cell precursors repopulating the posttransplant marrow. The expression of CD10 and CD19 antigens during early B-cell ontogeny post-BMT preceded the expression of CD20, CD21, CD22, CD40, and sIgM. The surface antigen profiles of the emerging B-cell precursors were similar to those of fetal liver or fetal bone marrow B-cell precursors. Our comparisons of BM and PBL samples from patients in the early post- BMT period demonstrated that (1) PBL initially contains fewer B-lineage cells than does BM, and (2) circulating B-lineage lymphoid cells have a more mature immunophenotype than do BM B-lineage lymphoid cells. Comparison of the surface antigen profiles of day 30 versus day 100 or year 1 BM or PBL lymphoid cells showed an increase in the percentages of CD10+CD22- undifferentiated lymphocyte precursors, as well as CD19+sIgM- B-cell precursors (pre-pre-B), consistent with a time- dependent expansion of these B-cell precursor populations post-BMT. Importantly, the percentages of CD10+CD22+ and CD19+sIgM+ B-cell precursor (pre-B) populations also increased between 30 days and 1 year post-BMT, confirming the ability of emerging immature B-cell precursors to differentiate along the B-precursor pathway. The acquisition and expression of B-lineage differentiation antigens at different stages of the post-BMT B-cell ontogeny support the notion that the expression of these antigens is developmentally programmed. Similar to patients in previous autologous BMT studies, recipients of B-cell precursor- depleted autografts had normal or nearly normal serum immunoglobulin levels, suggesting that the maturing B-cell/plasma cell populations can produce and secrete immunoglobulins. The development of a functional CD19+ B-lineage lymphoid compartment in recipients of autografts which were depleted of CD19+ B-cell precursors corroborates the previously postulated existence of CD19- B-lineage lymphoid progenitor cells.
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LeBien, Tucker W. "Fates of human B-cell precursors." Blood 96, no. 1 (July 1, 2000): 9–23. http://dx.doi.org/10.1182/blood.v96.1.9.
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Abstract Development of mammalian B-lineage cells is characterized by progression through a series of checkpoints defined primarily by rearrangement and expression of immunoglobulin genes. Progression through these checkpoints is also influenced by stromal cells in the microenvironment of the primary tissues wherein B-cell development occurs, ie, fetal liver and bone marrow and adult bone marrow. This review focuses on the developmental biology of human bone marrow B-lineage cells, including perturbations that contribute to the origin and evolution of B-lineage acute lymphoblastic leukemia and primary immunodeficiency diseases characterized by agammaglobulinemia. Recently described in vitro and in vivo models that support development and expansion of human B-lineage cells through multiple checkpoints provide new tools for identifying the bone marrow stromal cell–derived molecules necessary for survival and proliferation. Mutations in genes encoding subunits of the pre-B cell receptor and molecules involved in pre-B cell receptor signaling culminate in X-linked and non–X-linked agammaglobulinemia. A cardinal feature of these immunodeficiencies is an apparent apoptotic sensitivity of B-lineage cells at the pro-B to pre-B transition. On the other end of the spectrum is the apoptotic resistance that accompanies the development of B-lineage acute lymphoblastic leukemia, potentially a reflection of genetic abnormalities that subvert normal apoptotic programs. The triad of laboratory models that mimic the bone marrow microenvironment, immunodeficiency diseases with specific defects in B-cell development, and B-lineage acute lymphoblastic leukemia can now be integrated to deepen our understanding of human B-cell development.
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LeBien, Tucker W. "Fates of human B-cell precursors." Blood 96, no. 1 (July 1, 2000): 9–23. http://dx.doi.org/10.1182/blood.v96.1.9.013k27_9_23.
Full textAbstract:
Development of mammalian B-lineage cells is characterized by progression through a series of checkpoints defined primarily by rearrangement and expression of immunoglobulin genes. Progression through these checkpoints is also influenced by stromal cells in the microenvironment of the primary tissues wherein B-cell development occurs, ie, fetal liver and bone marrow and adult bone marrow. This review focuses on the developmental biology of human bone marrow B-lineage cells, including perturbations that contribute to the origin and evolution of B-lineage acute lymphoblastic leukemia and primary immunodeficiency diseases characterized by agammaglobulinemia. Recently described in vitro and in vivo models that support development and expansion of human B-lineage cells through multiple checkpoints provide new tools for identifying the bone marrow stromal cell–derived molecules necessary for survival and proliferation. Mutations in genes encoding subunits of the pre-B cell receptor and molecules involved in pre-B cell receptor signaling culminate in X-linked and non–X-linked agammaglobulinemia. A cardinal feature of these immunodeficiencies is an apparent apoptotic sensitivity of B-lineage cells at the pro-B to pre-B transition. On the other end of the spectrum is the apoptotic resistance that accompanies the development of B-lineage acute lymphoblastic leukemia, potentially a reflection of genetic abnormalities that subvert normal apoptotic programs. The triad of laboratory models that mimic the bone marrow microenvironment, immunodeficiency diseases with specific defects in B-cell development, and B-lineage acute lymphoblastic leukemia can now be integrated to deepen our understanding of human B-cell development.
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McGowan, Neil W. A., Emily J. Walker, Heather Macpherson, Stuart H. Ralston, and Miep H. Helfrich. "Cytokine-Activated Endothelium Recruits Osteoclast Precursors." Endocrinology 142, no. 4 (April 1, 2001): 1678–81. http://dx.doi.org/10.1210/endo.142.4.8204.
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Abstract Osteoclast precursors reach sites of osteoclast formation and remodelling via the vasculature and are therefore destined to encounter endothelium before migrating to the bone surface. Here we investigated the hypothesis that endothelium may be involved in the regulation of osteoclast precursor recruitment to sites of bone resorption. Osteoclast precursors in human peripheral blood were identified by their ability to form mature osteoclasts in 21-day cultures supplemented with RANKLigand, M-CSF, 1,25(OH)2-vitamin D3, dexamethasone and prostaglandin E2. Under control conditions few osteoclast precursors adhered to endothelial cells (the human bone marrow-derived endothelial cell line BMEC-1). However, BMEC-1 cells treated with the resorption stimulating cytokines IL-1β and TNFα depleted the PBMC population of all osteoclast precursors. These results provide the first evidence that osteoclast precursors can adhere to endothelium and suggest that endothelium could play an important role in the recruitment of osteoclast precursors to sites of bone resorption.
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Varnum-Finney, Barbara, Louise E. Purton, Monica Yu, Carolyn Brashem-Stein, David Flowers, Steven Staats, Kateri A. Moore, et al. "The Notch Ligand, Jagged-1, Influences the Development of Primitive Hematopoietic Precursor Cells." Blood 91, no. 11 (June 1, 1998): 4084–91. http://dx.doi.org/10.1182/blood.v91.11.4084.
Full textAbstract:
Abstract We examined the expression of two members of theNotch family, Notch-1 and Notch-2, and one Notch ligand, Jagged-1, in hematopoietic cells. Both Notch-1 and Notch-2 were detected in murine marrow precursors (Lin−Sca-1+c-kit+). The Notch ligand, Jagged-1, was not detected in whole marrow or in precursors. However, Jagged-1 was seen in cultured primary murine fetal liver stroma, cultured primary murine bone marrow stroma, and in stromal cell lines. These results indicate a potential role for Notch-Notch ligand interactions in hematopoiesis. To further test this possibility, the effect of Jagged-1 on murine marrow precursor cells was assessed by coculturing sorted precursor cells (Lin−Sca-1+c-kit+) with a 3T3 cell layer that expressed human Jagged-1 or by incubating sorted precursors with beads coated with the purified extracellular domain of human Jagged-1 (Jagged-1ext). We found that Jagged-1, presented both on the cell surface and on beads, promoted a twofold to threefold increase in the formation of primitive precursor cell populations. These results suggest a potential use for Notch ligands in expanding precursor cell populations in vitro.
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Varnum-Finney, Barbara, Louise E. Purton, Monica Yu, Carolyn Brashem-Stein, David Flowers, Steven Staats, Kateri A. Moore, et al. "The Notch Ligand, Jagged-1, Influences the Development of Primitive Hematopoietic Precursor Cells." Blood 91, no. 11 (June 1, 1998): 4084–91. http://dx.doi.org/10.1182/blood.v91.11.4084.411k05_4084_4091.
Full textAbstract:
We examined the expression of two members of theNotch family, Notch-1 and Notch-2, and one Notch ligand, Jagged-1, in hematopoietic cells. Both Notch-1 and Notch-2 were detected in murine marrow precursors (Lin−Sca-1+c-kit+). The Notch ligand, Jagged-1, was not detected in whole marrow or in precursors. However, Jagged-1 was seen in cultured primary murine fetal liver stroma, cultured primary murine bone marrow stroma, and in stromal cell lines. These results indicate a potential role for Notch-Notch ligand interactions in hematopoiesis. To further test this possibility, the effect of Jagged-1 on murine marrow precursor cells was assessed by coculturing sorted precursor cells (Lin−Sca-1+c-kit+) with a 3T3 cell layer that expressed human Jagged-1 or by incubating sorted precursors with beads coated with the purified extracellular domain of human Jagged-1 (Jagged-1ext). We found that Jagged-1, presented both on the cell surface and on beads, promoted a twofold to threefold increase in the formation of primitive precursor cell populations. These results suggest a potential use for Notch ligands in expanding precursor cell populations in vitro.
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Caldwell, Charles W., Edward Poje, and Mary A. Helikson. "B-Cell Precursors in Normal Pediatric Bone Marrow." American Journal of Clinical Pathology 95, no. 6 (June 1, 1991): 816–23. http://dx.doi.org/10.1093/ajcp/95.6.816.
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Hayashi, Shin-Ichi, Akitomo Miyamoto, Toshiyuki Yamane, Hiroshi Kataoka, Minetaro Ogawa, Seiichi Sugawara, Satomi Nishikawa, et al. "Osteoclast precursors in bone marrow and peritoneal cavity." Journal of Cellular Physiology 170, no. 3 (March 1997): 241–47. http://dx.doi.org/10.1002/(sici)1097-4652(199703)170:3<241::aid-jcp4>3.0.co;2-o.
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Kapasi, Zoher F., Dahui Qin, William G. Kerr, Marie H. Kosco-Vilbois, Leonard D. Shultz, John G. Tew, and Andras K. Szakal. "Follicular Dendritic Cell (FDC) Precursors in Primary Lymphoid Tissues." Journal of Immunology 160, no. 3 (February 1, 1998): 1078–84. http://dx.doi.org/10.4049/jimmunol.160.3.1078.
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Abstract The origin of follicular dendritic cells (FDC) is unresolved, and as such, remains controversial. Based on the migration of Ag-transporting cells (ATC) into lymphoid follicles and the phenotypic similarity between FDC and ATC, one hypothesis is that ATC may represent emigrating FDC precursors. This contrasts with the view that FDC originate from local stromal cells in the secondary lymphoid tissues. Mice homozygous for the severe combined immunodeficiency (prkdcscid) mutation (scid) lack FDC. Thus, they provide a powerful tool for assessing de novo generation of FDC. To test whether FDC precursors could be found in bone marrow or fetal liver, scid/scid mice were reconstituted with either: 1) bone marrow cells from (BALB/c × C57BL/6)F1 donors, 2) bone marrow cells from ROSA BL/6 F1 (lacZ-transfected) mice, 3) rat bone marrow cells, or 4) rat fetal liver cells. Six to eight weeks after reconstitution with F1 bone marrow, cells reactive with the FDC-labeling mAb, FDC-M1, also expressed donor class I molecules on their surfaces. Similarly in mice reconstituted with lacZ-transfected bone marrow cells, these cells were also positive for the lacZ gene product. Furthermore, in spleens of animals reconstituted with either rat bone marrow or rat fetal liver, rat FDC were identified using the specifically labeling mAb, ED5. In all cases, host FDC were also present, indicating that scid/scid mice have FDC precursors that will mature in the presence of allogeneic or xenogeneic lymphoid cells. In summary, FDC can be derived from progenitor cells present in primary lymphoid tissues.
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Compston, JE. "Bone marrow and bone: a functional unit." Journal of Endocrinology 173, no. 3 (June 1, 2002): 387–94. http://dx.doi.org/10.1677/joe.0.1730387.
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Bone and bone marrow, although often regarded as separate systems, function as a single unit. Cells in the bone marrow are the precursors of bone remodelling cells and exert an important regulatory role both on their own development and the remodelling process, acting as mediators for the effects of systemic and local factors. Other cells, such as immune cells and megakaryocytes, also contribute to the regulation of bone cell development and activity. Many diseases that affect the bone marrow have profound effects on bone, involving interactions between abnormal and normal marrow cells and those of bone. Although recent advances in bone physiology have produced new insights into the relationship between bone marrow and bone cells, much remains to be learnt about the mechanisms by which marrow and bone act in synergy to regulate bone remodelling, both in health and disease.
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Wolf, Sarah, Bonnie Blomberg, and Richard Riley. "Aged mice demonstrate altered regulation of distinct B cell developmental pathways (85.10)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S120. http://dx.doi.org/10.4049/jimmunol.178.supp.85.10.
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Abstract Three precursor subsets in bone marrow that generate new B cells were identified in young and aged (20–22 mo.) adult mice. The major subset (c-kit neg) is reduced in aged mice while minor c-kit+ and B1 lineage precursors are better maintained. In vitro, the c-kit+ and B1 precursors more readily generate B cells that undergo spontaneous activation. We suggest that altered levels of these precursors contribute to changes in B cell production and bias to activated phenotypes in aged mice. The “aged phenotype” of few c-kit neg, but maintained c-kit+/B1 precursors, is mimicked in young adult lambda 5 gene knockout mice as are the alterations in new B cell development. Therefore, the preBCR promotes development of c-kit neg B cell precursors, but is not necessary for c-kit+ and B1 precursors. Lambda 5 is decreased in aged B cell precursors, together with E2A. This suggests the hypothesis that, in aged mice, poor preBCR expression interferes with development of c-kit neg B precursors, but not c-kit+/B1 precursors. This, in turn, contributes to changes in the number, specificity, and function of new B cells generated in senescent bone marrow. Supported by NIH grants AI 064591 and AG 025256 to RLR
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Xu, Jing, Song-Chang Lin, Jiyuan Chen, Yuanxin Miao, George E. Taffet, Mark L. Entman, and Yanlin Wang. "CCR2 mediates the uptake of bone marrow-derived fibroblast precursors in angiotensin II-induced cardiac fibrosis." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 2 (August 2011): H538—H547. http://dx.doi.org/10.1152/ajpheart.01114.2010.
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Angiotensin II plays an important role in the development of cardiac hypertrophy and fibrosis, but the underlying cellular and molecular mechanisms are not completely understood. Recent studies have shown that bone marrow-derived fibroblast precursors are involved in the pathogenesis of cardiac fibrosis. Since bone marrow-derived fibroblast precursors express chemokine receptor, CCR2, we tested the hypothesis that CCR2 mediates the recruitment of fibroblast precursors into the heart, causing angiotensin II-induced cardiac fibrosis. Wild-type and CCR2 knockout mice were infused with angiotensin II at 1,500 ng·kg−1·min−1. Angiotensin II treatment resulted in elevated blood pressure and cardiac hypertrophy that were not significantly different between wild-type and CCR2 knockout mice. Angiotensin II treatment of wild-type mice caused prominent cardiac fibrosis and accumulation of bone marrow-derived fibroblast precursors expressing the hematopoietic markers, CD34 and CD45, and the mesenchymal marker, collagen I. However, angiotensin II-induced cardiac fibrosis and accumulation of bone marrow-derived fibroblast precursors in the heart were abrogated in CCR2 knockout mice. Furthermore, angiotensin II treatment of wild-type mice increased the levels of collagen I, fibronectin, and α-smooth muscle actin in the heart, whereas these changes were not observed in the heart of angiotensin II-treated CCR2 knockout mice. Functional studies revealed that the reduction of cardiac fibrosis led to an impairment of cardiac systolic function and left ventricular dilatation in angiotensin II-treated CCR2 knockout mice. Our data demonstrate that CCR2 plays a pivotal role in the pathogenesis of angiotensin II-induced cardiac fibrosis through regulation of bone marrow-derived fibroblast precursors.
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Ikuta, K., and I. L. Weissman. "The junctional modifications of a T cell receptor gamma chain are determined at the level of thymic precursors." Journal of Experimental Medicine 174, no. 5 (November 1, 1991): 1279–82. http://dx.doi.org/10.1084/jem.174.5.1279.
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T precursors from fetal liver and adult bone marrow were compared for their ability to give rise to V gamma 4+ T cell development. Fetal thymic lobes were repopulated with fetal liver or adult bone marrow cells, and the organ-cultured thymocytes were analyzed for their T cell receptor expression by the polymerase chain reaction (PCR). Both day 14 fetal liver and adult bone marrow cells gave rise to thymocytes with V gamma 4-J gamma 1 transcripts. However, the average size of the PCR products derived from adult precursors was slightly larger than that from fetal precursors. DNA sequence analysis of the V gamma 4-J gamma 1 transcripts showed that early fetal liver precursors predominantly gave rise to thymocytes with the V gamma 4-J gamma 1 transcripts without N nucleotide insertion, while late fetal liver and adult marrow precursors predominantly gave rise to thymocytes with modified V gamma 4-J gamma 1 junctions. These results suggest the possibility that the level of the N nucleotide insertion is programmed at the level of thymic precursors. This study also supported the model presented previously that the developmental potential of hematopoietic stem cells may change during ontogeny.
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Batra, Reema, Thomas M. Herndon, Joao Ascensao, and Geraldine P. Schechter. "Ribavirin-Induced Dysplasia." Blood 108, no. 11 (November 16, 2006): 4861. http://dx.doi.org/10.1182/blood.v108.11.4861.4861.
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Abstract Ribavirin is a synthetic nucleoside analogue given with pegylated interferon alfa-2a for the treatment of hepatitis C. Hemolytic anemia has been reported in 10–15% of patients, usually within 1–2 weeks of the initiation of therapy. The pathogenesis of this phenomenon is unclear. Pegylated interferon alfa-2a has been associated with pancytopenia. We report two cases of ribavirin-induced anemia that are not due solely to hemolysis. Case A is a 56 year old African-American man, status post liver transplant in July 2005 for hepatitis C. He had a recurrence in February 2006, and was placed on ribavirin 1200 mg daily and pegylated interferon 1.8 micrograms weekly. Within 1 month, his hemoglobin dropped to 8.1 g/dL, his MCV was 107mm3 and his reticulocyte count was 57K per mm3, while maintaining a normal white blood cell and platelet count. His Coombs test was negative. There was no response to the administration of erythropoietin. Bone marrow aspirate and biopsy showed marked erythroid dysplasia - including multi-nucleated precursors and megaloblastosis. There was no morphological evidence of myeloid or megakaryocytic dysplasia. Cytogenetic studies revealed a normal male karyotype (46XY). Case B is a 58 year old African-American man with hepatitis C. In January 2006 he was started on ribavirin 1200 mg daily, in combination with pegylated interferon. Eight weeks later, he was found to have a hemoglobin of 8.1 g/dl - decreased from 12.2 g/dL. The MCV was 104.4 mm3, and the reticulocyte count was 56K per mm3. His Coombs test was negative. Bone marrow biopsy performed at that time showed similar findings to Case A. Ribavirin and pegylated interferon were discontinued; a repeat bone marrow after six weeks showed only minimal dyserythropoiesis. He is currently maintaining his hemoglobin between 12 and 13 g/dL, with no transfusion or erythropoietin support. There are no reported associations between ribavirin and erythroid dysplasia in humans. Ribavirin has been shown to have cytotoxic effects on bone marrows in animal models. In one study, ribavirin was given intraperitoneally to rats in doses ranging from 10 to 200 mg/kg 1. Bone marrow samples obtained at 24 and 48 hours demonstrated micronuclei in erythroid precursors, with recovery at 72 hours. Rhesus monkeys given ribavirin at doses of 30 or 100 mg/kg/day intramuscularly for 10 days developed a normocytic, normochromic anemia, which was severe in the high-dose group 2. The bone marrows demonstrated a marked decrease in late erythroid precursors, while the early precursors remained unchanged. There was also vacuolization of the erythroid precursors as well as erythrophagocytosis. No changes were noted in the myeloid precursor cells, and the megakaryocytes appeared increased. After discontinuation of treatment the hemoglobin returned to normal, demonstrating a reversible effect. The bone marrows of the patients demonstrate ineffective erythropoiesis with marked erythroid dysplasia and megaloblastosis. These findings are associated with a decreased proportion of cells in the DNA synthesis of the cell cycle, an increase in the fraction of late precursor cells undergoing apoptosis, and an interruption in mitosis. These findings may be due to ribavirin’s interference in the maturation of erythroid cells. These observations need to be confirmed in a prospective manner in a large cohort of patients; they also suggest the need for a more complete evaluation of anemia in patients treated with ribavirin.
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Merluzzi, V. J., P. A. Trail, and K. Last-Barney. "Differential expression of lymphokine-activated killer cells and natural killer cells in adoptive transfer experiments utilizing fractionated bone marrow." Journal of Immunology 137, no. 8 (October 15, 1986): 2425–27. http://dx.doi.org/10.4049/jimmunol.137.8.2425.
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Abstract Precursors of murine natural killer (NK) cells and lymphokine-activated killer (LAK) cells can be distinguished by utilizing an adoptive transfer system in which donor bone marrow is fractionated on Percoll discontinuous gradients. Although precursors of LAK cells are present in all fractions, one fraction (greater than 65% Percoll) contains LAK precursors and is depleted of NK precursors. Both in vitro NK activity and in vivo hybrid resistance is abrogated in recipients of bone marrow from the greater than 65% Percoll fraction, whereas LAK activity can be readily demonstrated.
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Kotton, Darrell N., Bei Yang Ma, Wellington V. Cardoso, Elisabeth A. Sanderson, Ross S. Summer, Mary C. Williams, and Alan Fine. "Bone marrow-derived cells as progenitors of lung alveolar epithelium." Development 128, no. 24 (December 15, 2001): 5181–88. http://dx.doi.org/10.1242/dev.128.24.5181.
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We assessed the capacity of plastic-adherent cultured bone marrow cells to serve as precursors of differentiated parenchymal cells of the lung. By intravenously delivering lacZ-labeled cells into wild-type recipient mice after bleomycin-induced lung injury, we detected marrow-derived cells engrafted in recipient lung parenchyma as cells with the morphological and molecular phenotype of type I pneumocytes of the alveolar epithelium. At no time after marrow cell injection, did we detect any engraftment as type II pneumocytes. In addition, we found that cultured and fresh aspirates of bone marrow cells can express the type I pneumocyte markers, T1α and aquaporin-5. These observations challenge the current belief that adult alveolar type I epithelial cells invariably arise from local precursor cells and raise the possibility of using injected marrow-derived cells for therapy of lung diseases characterized by extensive alveolar damage.
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Bodi, Estevão, Sandra P. Hurtado, Marcelo A. Carvalho, Radovan Borojevic, and Antônio C. Campos de Carvalho. "Gap junctions in hematopoietic stroma control proliferation and differentiation of blood cell precursors." Anais da Academia Brasileira de Ciências 76, no. 4 (December 2004): 743–56. http://dx.doi.org/10.1590/s0001-37652004000400009.
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We examined gap junction communication in an in vitro model of hematopoiesis, using the murine bone marrow stroma cell line S-17, and primary cultures of murine marrow-derived blood cell precursors. S-17 cells express several connexins, the major one being connexin 43. Connexin expression and formation of functional gap junctions is modulated by stroma cell density. Transfection of S-17 cells with a vector containing connexin 43 sense or anti-sense sequences increased or decreased, respectively, connexin 43 synthesis and intercellular dye coupling. Under these conditions, modulation of gap junction-mediated communication modified the growth pattern of stroma itself, as well as the ability of the stroma to sustain hematopoiesis. Increased connexin 43 expression was associated with a delay in differentiation of blood cells, resulting in increased production of hematopoietic precursors, while decreased connexin 43 expression elicited an accelerated differentiation of myeloid blood cell precursor cells. These results suggest that connexin-mediated coupling in the stroma modulates the ratio between proliferation and differentiation of hematopoietic precursors. We therefore propose that increased gap junction communication in the stroma elicits an enhanced production of immature bone marrow cells through the delay in their terminal differentiation, inducing consequently an extended proliferation period of blood cell precursors.
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Kouro, Taku, Vinay Kumar, and Paul W. Kincade. "Relationships between early B- and NK-lineage lymphocyte precursors in bone marrow." Blood 100, no. 10 (November 15, 2002): 3672–80. http://dx.doi.org/10.1182/blood-2002-02-0653.
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Recent studies have demonstrated that lineage marker–negative (Lin−) c-kitLo Flk-2/Flt3+IL-7R+ Sca-1Lo CD27+Ly-6C− Thy-1−CD43+CD16/32Lo/− terminal deoxynucleotidyl transferase (TdT)+ cells in murine bone marrow are functional lymphocyte precursors. However, it has not been clear if this is an obligate intermediate step for transit of multipotential hematopoietic stem cells to natural killer (NK) cells. We have now used serum-free, stromal cell–free cultures to determine that NK progenitors are enriched among an estrogen-regulated, c-kitLo subset of the Lin− fraction. However, several experimental approaches suggested that this population is heterogeneous and likely represents a stage where B and NK lineages diverge. Although most B-cell precursors were directly sensitive to estrogen in culture, much of the NK-cell precursor activity in that fraction was hormone resistant. B-lineage potential was largely associated with interleukin 7 receptor α (IL-7Rα) expression and was selectively driven in culture by IL-7. In contrast, many NK precursors did not display detectable amounts of this receptor and their maturation was selectively supported by IL-15. Finally, single-cell experiments showed that the Lin−c-kitLo fraction contains a mixture of B/NK, B-restricted, and NK-restricted progenitors. Two-step culture experiments revealed that NK precursors become hormone resistant on or before acquisition of CD122, signaling commitment to the NK lineage. CD45R is preferentially, but not exclusively, expressed on maturing B-lineage cells. Production of these 2 blood cell types is regulated in bone marrow by common and then independent mechanisms that can now be studied with greater precision.
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Szabo, Paul, Kesheng Zhao, Irena Kirman, Joel Le Maoult, Rubendra Dyall, William Cruikshank, and Marc E. Weksler. "Maturation of B Cell Precursors Is Impaired in Thymic-Deprived Nude and Old Mice." Journal of Immunology 161, no. 5 (September 1, 1998): 2248–53. http://dx.doi.org/10.4049/jimmunol.161.5.2248.
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Abstract We have previously reported that bone marrow B cell precursors from thymic-deprived nude and old mice express less recombination-activating gene-1 (RAG-1) mRNA than they do in young euthymic mice. We now report that both nude and old mice have decreased bone marrow pre-B cells and that fewer pre-B cells express RAG protein. This combination of events appears to be the basis for the lower level of bone marrow RAG mRNA in thymic-deprived mice. A link between thymic function and B cell development was suggested by the similar kinetics of thymic involution and of declining bone marrow RAG-1 gene expression during aging. Support for this hypothesis was obtained by demonstrating that injection of supernatant medium from activated CD8+ but not CD4+ young T cells from mice increases RAG mRNA, RAG protein, and the number of bone marrow pre-B cells in nude and old mice. Furthermore, in vivo CD8+ T cells also regulate bone marrow RAG gene expression. Thus, mice deficient in CD8+ T cells expressed levels of RAG-1 mRNA in their bone marrow that were only 10% of those observed in normal or CD4+ T cell-deficient mice. IL-16 was detected in the supernatant medium from activated T cell cultures, and injection of nanogram quantities of recombinant IL-16 (rIL-16) into nude or old mice increased the levels of RAG mRNA in bone marrow B cell precursors and the number of bone marrow pre-B cells. We conclude that the impaired development of B cells within the bone marrow of thymic-deprived nude and old mice can be reversed, at least in part, by the administration of rIL-16.
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Chervenak, R., J. W. Moorhead, and J. J. Cohen. "Prethymic T cell precursors express receptors for antigen." Journal of Immunology 134, no. 2 (February 1, 1985): 695–98. http://dx.doi.org/10.4049/jimmunol.134.2.695.
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Abstract An anti-idiotype serum raised in BALB/c mice against syngeneic lymph node T cells from 2,4-dinitrofluorobenzene (DNFB)-sensitized mice was used to study the early expression of antigen receptors on developing T cells. Normal BALB/c bone marrow cells were treated with either anti-Thy-1.2 plus complement or anti-Thy-1.2 and anti-idiotype plus complement before use in the reconstitution of lethally irradiated syngeneic mice. Five weeks after reconstitution, recipient mice were assayed for both contact sensitivity (CS) and in vitro proliferative responses to DNFB. Mice reconstituted with bone marrow cells treated with both anti-Thy and anti-idiotype sera showed a significant decrease in reactivity to DNFB in both assay systems when compared with mice reconstituted with marrow treated with anti-Thy only. CS response to the noncross-reacting hapten oxazolone was identical in both recipient groups. Bone marrow mixing experiments showed no evidence of anti-idiotype-induced suppressor cells in these experiments. These data provide strong evidence that at least some T cell precursors express receptors for antigen prethymically.
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Worthley, Daniel L., Yiling Si, Michael Quante, Michael Churchill, Siddhartha Mukherjee, and Timothy C. Wang. "Bone marrow cells as precursors of the tumor stroma." Experimental Cell Research 319, no. 11 (July 2013): 1650–56. http://dx.doi.org/10.1016/j.yexcr.2013.03.006.
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Iijima, N., M. M. Linehan, S. Saeland, and A. Iwasaki. "Vaginal epithelial dendritic cells renew from bone marrow precursors." Proceedings of the National Academy of Sciences 104, no. 48 (November 15, 2007): 19061–66. http://dx.doi.org/10.1073/pnas.0707179104.
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Huang, Christene A., Cassis Henry, John Iacomini, Thereza Imanishi-Kari, and Henry H. Wortis. "Adult bone marrow contains precursors for CD5+ B cells." European Journal of Immunology 26, no. 10 (October 1996): 2537–40. http://dx.doi.org/10.1002/eji.1830261039.
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Zhang, Yi, Akihisa Harada, Jian-bin Wang, Yan-yun Zhang, Shin-ichi Hashimoto, Makoto Naito, and Kouji Matsushima. "Bifurcated Dendritic Cell Differentiation In Vitro From Murine Lineage Phenotype-Negative c-kit+ Bone Marrow Hematopoietic Progenitor Cells." Blood 92, no. 1 (July 1, 1998): 118–28. http://dx.doi.org/10.1182/blood.v92.1.118.413a01_118_128.
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We have recently established the culture system to generate dendritic cells (DCs) from murine Lin−c-kit+ bone marrow hematopoietic progenitor cells (HPCs) in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) + stem cell factor (SCF) + tumor necrosis factor-α (TNF-α). We present here the identification of two DC precursor subsets originated from HPCs with the phenotype of CD11b−/dullCD11c+ and CD11b+hiCD11c+ that develop independently at early time points (days 4 to 6) in the same culture conditions. Both of CD11b−/dullCD11c+ and CD11b+hiCD11c+ precursors could differentiate at day 10 to 14 into CD11b−/dullCD11c+ mature DCs with typical morphology, phenotype, and the ability to stimulate allogenic mixed leukocyte reaction (MLR). However, the endocytic capacity of fluorescein isothiocyanate-dextran was markedly reduced during the differentiation. CD11b−/dullCD11c+precursors expressed high levels of Ia, CD86, CD40, and E-cadherin molecules, but not c-fms transcript, and mature DCs derived from this precursor subset continue to express abundant E-cadherin antigen, a discernible marker for Langerhans cells. In contrast, CD11b+hiCD11c+ precursors expressed c-fms mRNA, but low levels of Ia, CD86, and E-cadherin, whereas CD40 was undetectable. CD11b−/dullCD11c+mature DCs differentiated from these precursors displayed abundant c-fms mRNA and nonspecific esterase activity. Interestingly, CD11b+hiCD11c+precursors, but not CD11b−/dullCD11c+precursors, may be bipotent cells that can be induced by M-CSF to differentiate into macrophages. All of these results suggest that CD11b−/dullCD11c+ and CD11b+hiCD11c+ cells are distinct DC precursors derived from Lin−c-kit+ HPCs, which differentiate into mature DCs through bifurcated and independent DC differentiation pathways.
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Mossalayi, MD, JC Lecron, P. Goube de Laforest, G. Janossy, P. Debre, and J. Tanzer. "Characterization of prothymocytes with cloning capacity in human bone marrow." Blood 71, no. 5 (May 1, 1988): 1281–87. http://dx.doi.org/10.1182/blood.v71.5.1281.1281.
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Abstract The identity of human bone marrow (BM)-derived T cell precursors with colony forming capacity has led to controversy because of contamination with mature clonogenic T cells. We achieved 2 Log elimination of mature T cells from BM using a cocktail of monoclonal antibodies: CD2, CD3, CD4, CD6, and CD8 followed by two successive baby rabbit C' treatment. T cell depleted BM can generate colonies of CD2+, CD3+, Ti+, mostly CD4+, in the presence of PHA, rIL2, and a prothymocyte differentiating activity derived from phytohemagglutinin (PHA) induced mononuclear cells. These precursors could be enriched three- to sixfold by percoll gradient centrifugation and then significantly bypass the number of contaminant mature T cells as shown by limiting dilution analysis. Colony generation by marrow precursors was inhibited by the addition of autologous T cells. This inhibition was mostly caused by the T8+ subset. CFU-TL growth was dramatically inhibited by eliminating CD7+ cells suggesting their positivity for this surface marker. These precursors needed major histocompatibility complex (MHC) II-positive cells for optimal growth but lack DR themselves.
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Mossalayi, MD, JC Lecron, P. Goube de Laforest, G. Janossy, P. Debre, and J. Tanzer. "Characterization of prothymocytes with cloning capacity in human bone marrow." Blood 71, no. 5 (May 1, 1988): 1281–87. http://dx.doi.org/10.1182/blood.v71.5.1281.bloodjournal7151281.
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The identity of human bone marrow (BM)-derived T cell precursors with colony forming capacity has led to controversy because of contamination with mature clonogenic T cells. We achieved 2 Log elimination of mature T cells from BM using a cocktail of monoclonal antibodies: CD2, CD3, CD4, CD6, and CD8 followed by two successive baby rabbit C' treatment. T cell depleted BM can generate colonies of CD2+, CD3+, Ti+, mostly CD4+, in the presence of PHA, rIL2, and a prothymocyte differentiating activity derived from phytohemagglutinin (PHA) induced mononuclear cells. These precursors could be enriched three- to sixfold by percoll gradient centrifugation and then significantly bypass the number of contaminant mature T cells as shown by limiting dilution analysis. Colony generation by marrow precursors was inhibited by the addition of autologous T cells. This inhibition was mostly caused by the T8+ subset. CFU-TL growth was dramatically inhibited by eliminating CD7+ cells suggesting their positivity for this surface marker. These precursors needed major histocompatibility complex (MHC) II-positive cells for optimal growth but lack DR themselves.
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Parsons, Christopher H., Barbara Szomju, and Dean H. Kedes. "Susceptibility of human fetal mesencyhmal stem cells to Kaposi sarcoma-associated herpesvirus." Blood 104, no. 9 (November 1, 2004): 2736–38. http://dx.doi.org/10.1182/blood-2004-02-0693.
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Abstract Recent reports link Kaposi sarcoma-associated herpesvirus (KSHV) infection of bone marrow cells to bone marrow failure and lymphoproliferative syndromes. The identity of the infected marrow cells, however, remains unclear. Other work has demonstrated that circulating mononuclear cells can harbor KSHV where its detection predicts the onset and severity of Kaposi sarcoma. In either setting, bone marrow precursors may serve as viral reservoirs. Since mesenchymal stem cells (MSCs) in human bone marrow regulate the differentiation and proliferation of adjacent hematopoietic precursors, we investigated their potential role in KSHV infection. Our results indicate that primary MSCs are susceptible to both cell-free and cell-associated KSHV in culture. Moreover, infection persisted within nearly half of the cells for up to 6 weeks. Thus, MSCs possess a clear capacity to support KSHV infection and warrant further exploration into their potential role in KSHV-related human disease. (Blood. 2004;104:2736-2738)