Copper
Judy A. Driskell, Ira Wolinsky in Sports Nutrition, 2005
The increase in the ratio of immature cells to mature granulocytes in the bone marrow of copper-deficient patients suggests that copper deficiency arrests the differentiation of neutrophils. Neutrophils and all other blood cells arise from a common parent cell, the pluripotent hematopoietic stem cell, in the bone marrow. The pluripotent stem cell differentiates into a myeloid progenitor cell called the colony forming unit-GEMM (CFU-GEMM) that further differentiates into colony forming units for erythrocytes (CFU-E), platelets (CFU-MEG), granulocytes (CFU-GM) and monocytes (CFU-M). The CFU-GM gives rise to the myeloblast that further differentiates into the promyelocyte, which becomes either the neutrophilic myelocyte, the eosinophilic myelocyte, or the basophilic myelocyte. Neutrophilic myelocytes differentiate through a pathway that has several stages that give rise to the metamyelocyte, the banded neutrophil and the segmented neutrophil. Presently, there are only a few reports showing that copper deficiency perturbs this pathway for neutrophil differentiation.
Cellular Components of Blood
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The PHSCs give rise to all mature blood cells that circulate freely in the peripheral blood. The stem cells undergo cell division and maturation in the bone marrow. The erythroid, granulocytic and megakaryocytic cell lines are derived from a common pluripotential stem cell, appearing as an early myeloid precursor called CFUGEMM (colony-forming unit, granulocyte, erythrocyte, monocyte and megakaryocyte). The precursor cells are stimulated by haemopoietic growth factors, resulting in considerable amplification within the system and increased production of one or more cell lines in accordance to need. The bone marrow is also the primary origin of lymphocytes, and there is some evidence for a common precursor cell for both myeloid and lymphoid cells (Figure 51.1).
Effects of rhlL-7 on Leukocyte Subsets in Mice: Implications for Antitumor Activity
Ronald H. Goldfarb, Theresa L. Whiteside in Tumor Immunology and Cancer Therapy, 2020
Interleukin 7 (IL-7) is a 25 kDa glycoprotein that was originally characterized as a product of a cloned murine bone marrow stromal cell line (1,2), and its mRNA has since been detected in the thymus and spleen (3). Human and murine recombinant IL-7 exhibit a 60% homology at the protein level with all of the six cysteine residues conserved (4). in vitro, IL-7 induces the proliferation of pro-B and pre-B lymphocytes (1,2) and affects the growth of both immature and mature cells of the T lymphocyte lineage (5–9). IL-7 also induces lymphokine-activated killer (LAK) activity from human peripheral blood leukocytes (9,10) and mouse splenocytes (11) in vitro. Further, IL-7 affects myeloid progenitor cells since splenic granulocyte-macrophage colony forming units (CFU-GM) and multipotential CFU (CFU-GEMM) are increased in mice treated with IL-7 (12,13), while total bone marrow CFU are decreased (13). Thus, the aims of these studies are to 1) determine whether the administration of recombinant human IL-7 (rhlL-7) to mice could alter the incidence or total number of various lymphoid subsets and 2) assess the effects of IL-7 against experimental metastases in mice.
The bone marrow stromal niche: a therapeutic target of hematological myeloid malignancies
Published in Expert Opinion on Therapeutic Targets, 2020
Lena Behrmann, Jasmin Wellbrock, Walter Fiedler
Myeloid malignancies are heterogeneous disorders characterized by uncontrolled proliferation of undifferentiated myeloid progenitor cell clones [1]. They result from genetic and epigenetic alterations in hematopoietic stem and progenitor cells (HSPCs), which perturb key processes such as proliferation, differentiation and self-renewal. Not infrequently, acute leukemias evolve from chronic stages like myelodysplastic syndrome (MDS), myeloproliferative neoplasms (MPNs) and chronic myelomonocytic leukemia (CMML) [2,3]. A relationship network is shown in Figure 1. MDS is characterized by ineffective hematopoiesis, leading to various cytopenias and dysplastic changes of developing blood cell progenitors. In contrast, MPNs are characterized by an excess of mature cells by uncontrolled proliferation from one or more of the myeloid lineages.
Microglia as therapeutic targets after neurological injury: strategy for cell therapy
Published in Expert Opinion on Therapeutic Targets, 2021
M. Collins Scott, Supinder S. Bedi, Scott D. Olson, Candice M. Sears, Charles S. Cox
While both are phagocytic cells, there are differences between microglia and macrophages. Microglia are derived from yolk sac erythromyeloid precursors. These precursor cells change to yolk sac pre-macrophages, which can migrate to the embryonic brain prior to the development of the BBB. After this migration, these pre-macrophages develop into microglia. Once the BBB has developed, yolk sac pre-macrophages that did not migrate and fetal liver monocytes can migrate and develop into peripheral tissue resident macrophages [1]. Monocytes originate in the bone marrow from the myeloid progenitor cell line [109]. Microglia in the resting state can be distinguished by low levels of CD45 expression, but in the midst of neuroinflammation, CD45 expression increases [109]. Other markers distinguish microglia from peripheral phagocytes, such as P2Y12 and transmembrane protein 119 (TMEM119). Monocytes and macrophages express Ly-6 c at varying levels, depending on their polarization; this marker can be used to distinguish peripheral cells having migrated to injury site [104]. Given these structural differences, it is important to be able to distinguish microglia from peripheral monocytes and macrophages [107,108,110,111].
Prophylaxis and treatment strategies for optimizing chemotherapy relative dose intensity
Published in Expert Review of Anticancer Therapy, 2021
Michelle Shayne, R. Donald Harvey, Gary H. Lyman
Romyelocel-L is a cryopreserved, off-the-shelf human allogeneic myeloid progenitor cell therapeutic manufactured by ex vivo expansion of CD34+ cells isolated from G-CSF–mobilized peripheral blood from healthy donors. The cells are intended to engraft transiently and produce effector cells that migrate to tissues damaged by chemotherapy. In a randomized phase 2 study in 160 acute myeloid leukemia patients treated with standard 7 + 3 induction/consolidation or high-dose cytarabine chemotherapy, romyelocel-L combined with G-CSF reduced infections, antibiotics use, and the length of hospitalization when compared to G-CSF use alone. The safety profile was generally similar between the two arms, including an equal incidence of febrile neutropenia [130].
Related Knowledge Centers
- Haematopoiesis
- Megakaryocyte
- Myeloid Tissue
- Granulocyte
- Hematopoietic Stem Cell
- Cellular Differentiation
- Red Blood Cell
- Monocyte
- Progenitor Cell
- Eosinophil