Disease relevance of Myeloid Cells

• Mouse myeloid leukemic cells which differ in their competence to be induced to differentiate by the normal macrophage- and granulocyte-inducing protein MGI have been used to study the relationship between type C RNA virus production and myeloid cell differentiation [1].
• The association between alkylating agent exposure and acute nonlymphocytic leukemia in humans indicates that myeloid cells may be particularly susceptible to mutagenic damage [2].
• In this study, we analyzed the mechanism by which a Stat3 deficiency in myeloid cells led to the induction of chronic enterocolitis in vivo [3].
• We previously generated a transgenic mouse model for acute promyelocytic leukemia (APL) by expressing the promyelocytic leukemia (PML)-retinoic acid receptor (RARalpha) cDNA in early myeloid cells [4].
• Crosslinking of p75/AIRM-1 or CD33 has been shown to sharply inhibit the in vitro proliferation of both normal myeloid cells and chronic myeloid leukemias [5].

High impact information on Myeloid Cells

• We also review the evidence supporting a model for a functional LPS receptor of myeloid cells, which is multimeric, comprised of GPI-anchored CD14 and a presently unidentified transmembrane protein that together bind LPS and initiate cell activation via kinase cascades [6].
• In the three years since its discovery, the pleiotropic cytokine interleukin-10 (IL-10) has been implicated as an important regulator of the functions of lymphoid and myeloid cells [7].
• An SDF-1 trap for myeloid cells stimulates angiogenesis [8].
• Together, the data suggest a model for VEGF-programmed adult neovascularization highlighting the essential paracrine role of recruited myeloid cells and a role for SDF1 in their perivascular retention [9].
• Deleting IKKbeta in myeloid cells, however, results in a significant decrease in tumor size [10].

Chemical compound and disease context of Myeloid Cells

• These studies identify the localization of the oncogenic form of the abl gene product encoded by the Abelson murine leukemia virus in the nuclei of myeloid cells and the association of the v-Abl protein with the transcriptional regulator cyclic AMP response element-binding protein (CREB) [11].
• It is well known that all-trans-retinoic acid (ATRA) can induce myeloid cell differentiation in acute promyelocytic leukemia (APL) cells [12].
• Spectrum of toxicities of amino acid methyl esters for myeloid cells is determined by distinct metabolic pathways [13].
• These findings indicate that HIV infection in lymphocytic, monocytic, and myeloid cell lines leads to increased expression of glucose transporter 1 and consequent increased cellular vitamin C uptake [14].
• This was confirmed in the U937 myeloid cell line transfected with HIV LTR linked to a chloramphenicol acetyl transferase reporter gene [15].

Biological context of Myeloid Cells

• NF1 appears to function as a tumor-suppressor gene in immature myeloid cells [16].
• These data support a model in which the Src family kinases Hck and Fgr function as negative regulators of myeloid cell chemokine signaling by maintaining the tonic phosphorylation of PIR-B [17].
• By enhancing expression of certain cell-cycle genes, CREB appears to promote growth-factor-independent proliferation and survival of myeloid cells [18].
• GM-CSF promotes homeostasis of myeloid cells [19].
• A recently cloned zinc finger gene, MZF-1, was found to be preferentially expressed in myeloid cells [20].

Anatomical context of Myeloid Cells

• The anti-inflammatory effects of anti-Flt1 were attributable to reduced mobilization of bone marrow-derived myeloid progenitors into the peripheral blood; impaired infiltration of Flt1-expressing leukocytes in inflamed tissues; and defective activation of myeloid cells [21].
• Endothelial leukocyte adhesion molecule-1 (ELAM-1) is an endothelial cell adhesion molecule that allows myeloid cells to attach to the walls of blood vessels adjacent to sites of inflammation [22].
• We show that colonization of bone marrow by HSCs in addition to myeloid cells is severely impaired in SDF-1(-/-) embryos by a long-term repopulation assay [23].
• To study the role for ICSBP, a hematopoietic cell-specific transcription factor in myeloid cell development, the gene was introduced into myeloid progenitor cells established from ICSBP-/- mice [24].
• Thus BLIMP-1 is a key regulator of terminal differentiation in two separate hematopoietic lineages: myeloid cells and B lymphocytes [25].

Associations of Myeloid Cells with chemical compounds

• We describe a novel cytoplasmic tyrosine kinase, termed BPK (B cell progenitor kinase), which is expressed in all stages of the B lineage and in myeloid cells [26].
• P-selectin glycoprotein ligand 1 (PSGL-1) is a mucin-like glycoprotein expressed on the surface of myeloid cells and serves as the high affinity counterreceptor for P-selectin [27].
• Selective effects of cyclosporin A on colony-forming lymphoid and myeloid cells in man [28].
• Leukotriene B4 (LTB4) was originally described as a potent lipid myeloid cell chemoattractant, rapidly generated from innate immune cells, that activates leukocytes through the G protein-coupled receptor BLT1 [29].
• Retinoic acid has been shown to induce large accumulations of tissue transglutaminase in cultured myeloid cells [30].

Gene context of Myeloid Cells

• Involvement of the Jak-3 Janus kinase in signalling by interleukins 2 and 4 in lymphoid and myeloid cells [31].
• Finally, the recruitment of myeloid cells to inflammatory sites was found strongly impeded in Stat5-deficient mice [32].
• We demonstrate here that in uninfected cells, BAK is complexed with the anti-apoptotic BCL-2 family member Myeloid Cell Leukemia 1 (MCL-1) [33].
• Taken together, these data suggest that neurofibromin is required to downregulate Ras activation in myeloid cells exposed to GM-CSF [34].
• Immune interferon induces the receptor for monomeric IgG1 on human monocytic and myeloid cells [35].

Analytical, diagnostic and therapeutic context of Myeloid Cells

• In vitro and in vivo differentiation into B cells, T cells, and myeloid cells of primitive yolk sac hematopoietic precursor cells expanded > 100-fold by coculture with a clonal yolk sac endothelial cell line [36].
• The absence of contamination by myeloid cells was confirmed by the results of Western blot analysis of the proteins of the cell population studied: no MPO protein was detectable [37].
• Equivalent numbers of human B, T, and myeloid cells were obtained after transplantation of cells treated with or without neutralization of TGF-beta [38].
• In the present study, we investigated whether G-CSF signaling in immature normal and leukemic human myeloid cells diverges at the level of activation of signal transducers and activators of transcription (STAT) proteins [39].
• This was confirmed by electron microscopy. hCAP-18 is synthesized at the same stage of myeloid cell maturation as lactoferrin, and is efficiently targeted to granules [40].

References