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At least 415 records · Page 23Linked to original sources
PubMed2004

Immature dendritic cell transdifferentiation into osteoclasts: a novel pathway sustained by the rheumatoid arthritis microenvironment.

Dendritic cells (DCs), the mononuclear cells that initiate immune response, and osteoclasts, the multinucleated bone-resorbing cells, are derived from monocyte/macrophage precursor cells. Granulocyte-macrophage colony-stimulating factor and macrophage colony-stimulating factor (M-CSF) reciprocally regulate the differentiation of both lineages in mice. Using human monocyte-derived DCs generated in vitro, we show that immature DCs transdifferentiate into functional osteoclasts (OCs) in the presence of M-CSF and receptor activator of nuclear factor-kappaB ligand (RANKL). Transdifferentiation operates through fusion of intermediate adherent bipolar fusiform mononuclear cells expressing CD14, CD1a, and RANKL and able to induce RANKL(+) T-cell proliferation. Surprisingly, DC fusion in vitro is faster and more efficient than monocyte fusion to form multinucleated giant cells. The transdifferentiation process reported here supports the existence of a high cellular plasticity within differentiated myeloid phagocytes. Importantly, this process is greatly enhanced by rheumatoid arthritis synovial fluid and involves proinflammatory cytokines such as interleukin 1 or tumor necrosis factor alpha, as well as components of the extracellular matrix such as hyaluronic acid. Our data therefore suggest that DC-derived OCs may be directly involved in the osteolytic lesions observed in human inflammatory bone diseases such as rheumatoid arthritis or in particular forms of Langerhans cell histiocytosis, characterized by accumulation of immature skin DCs and chronic lytic bone lesions.

Adult↗
PubMed2007

Arginase 1 is expressed in myelocytes/metamyelocytes and localized in gelatinase granules of human neutrophils.

Arginase 1 (ARG1) metabolizes arginine, thus reducing the availability of arginine as a substrate for nitric oxide synthase (NOS). The decreased production of nitric oxide (NO) by NOS and the production of ornithine by ARG1 affect immune responses and tissue regeneration at sites of infection, respectively. We here demonstrate that ARG1 is synthesized in myelocytes/metamyelocytes and is stored in gelatinase granules. In accordance with this, activated neutrophils coreleased ARG1 and gelatinase to the extracellular environment on stimulation with phorbol-12-myristate 13-acetate (PMA), formyl-methionyl-leucyl-phenylalanine (fMLP), or tumor necrosis factor alpha (TNF-alpha). Overall, these findings define ARG1 as a genuine gelatinase granule protein and support a model in which activated neutrophils release ARG1 at sites of infection to modulate immune responses and promote tissue regeneration.

Arginase↗
PubMed2006

Myeloblast phenotypic changes in myelodysplasia. CD34 and CD117 expression abnormalities are common.

We used a new method of data presentation and analysis, termed antigen mapping, to characterize recurring myeloblast phenotypic abnormalities in a series of 28 cases of myelodysplastic syndrome (MDS), including refractory anemia with ringed sideroblasts (RARS), refractory anemia with multilineage dysplasia (RCMLD), and refractory anemia with excess blasts (RAEB). Abnormal patterns of CD34 and CD117 expression were present in 50% of RARS, 68% of RCMLD, and 100% of RAEB cases. The presence of decreased myeloblast CD45 density, increased CD13 and CD34 density, and increased expression of CD11c and CD4(dim) were MDS grade-related. There was a direct relationship between the number of myeloblast phenotypic abnormalities (phenotypic score) and MDS grade. The myeloblast phenotypic scores also were correlated highly with International Prognostic Scoring System scores and risk categories. We found the antigen mapping technique to be an efficient data presentation and analysis method for the detection of MDS-associated abnormalities of antigen distribution and density.

Aged↗
PubMed1992

Mechanisms of clozapine-induced agranulocytosis.

The aetiology of clozapine-induced agranulocytosis remains unknown. Leading candidates include an immune mechanism that is possibly complement- or drug-dependent and a toxic mechanism. We analysed these mechanisms by culturing the granulocyte precursor stem cell from the bone marrow in the presence of patients' serum, clozapine or clozapine metabolites. Studies with patients' serum failed to identify an immune mechanism. On the basis of our preliminary data, it appears that a toxic mechanism may be responsible, and this is more likely to be due to a metabolite than to clozapine itself. Further studies are required to determine the sensitivity of bone marrow precursors to these clozapine derivatives. For instance, prospective collection of serum will make it possible to evaluate whether high metabolite concentrations develop in sensitive individuals and whether they are responsible for agranulocytosis. If such elevated levels occur, further studies will be required to determine whether prospective monitoring will effectively identify patients at risk and ultimately prevent the onset of agranulocytosis by early discontinuation of the drug.

Agranulocytosis↗
PubMed2004

Meningeal relapse in a patient with acute promyelocytic leukemia: a case report and review of the literature.

The involvement of central nervous system is rare in acute promyelocytic leukemia (APL). We report a APL patient of a 41 yr-old Korean male who presented with fever and petechia. Complete molecular remission was achieved with all-trans retinoic acid (ATRA), idarubicin, and cytarabine. Ten months later, he complained of a mild headache. The results of the physical examination and the complete blood counts were normal. The examination of cerebrospinal fluid showed the presence of promyelocyte. Bone marrow studies showed cytogenetic remission but with molecular relapse. He was treated with intrathecal and systemic chemotherapy.

Adult↗
PubMed2006

Trends in recommendations of myelosuppressive chemotherapy for the treatment of breast cancer: evolution of the national comprehensive cancer network guidelines and the cooperative group studies.

Breast cancer, the most commonly occurring cancer in women in the United States, is the second most common cause of cancer-related mortality. Mortality rates in breast cancer have, however, declined by 2.3% per year from 1990 to 2001, partly because of the development of better chemotherapy agents and regimens, which have resulted in major changes in the standards of care. To study the changes in the past decade in expert opinion about the preferred chemotherapy for breast cancer, we compared the treatment guidelines of the National Comprehensive Cancer Network (NCCN) for 1996, 2000, and 2005. The myelotoxicity associated with the NCCN-recommended agents was also assessed by using data from the prescribing information for the drugs. This review showed that many of the agents, combinations of agents, and new dosing schedules currently recommended in the NCCN guidelines for the treatment of breast cancer are associated with myelosuppression. Many of these myelosuppressive regimens, which were used in the past to treat advanced-stage or metastatic disease, are now prescribed for early-stage disease. Furthermore, the cytotoxic agents and regimens recommended by the NCCN are more myelosuppressive than those recommended a decade ago. Many oncologists are aware of this trend toward the more intensive treatment of patients with cancer and take proactive steps to minimize the risk of myelosuppression and its complications.

Adult↗
PubMed2000

Vascular endothelial growth factor synergistically enhances bone morphogenetic protein-4-dependent lymphohematopoietic cell generation from embryonic stem cells in vitro.

The totipotent mouse embryonic stem (ES) cell is known to differentiate into cells expressing the beta-globin gene when stimulated with bone morphogenetic protein (BMP)-4. Here, we demonstrate that BMP-4 is essential for generating both erythro-myeloid colony-forming cells (CFCs) and lymphoid (B and NK) progenitor cells from ES cells and that vascular endothelial growth factor (VEGF) synergizes with BMP-4. The CD45(+) myelomonocytic progenitors and Ter119(+) erythroid cells began to be detected with 0.5 ng/mL BMP-4, and their levels plateaued at approximately 2 ng/mL. VEGF alone weakly elevated the CD34(+) cell population though no lymphohematopoietic progenitors were induced. However, when combined with BMP-4, 2 to 20 ng/mL VEGF synergistically augmented the BMP-4-dependent generation of erythro-myeloid CFCs and lymphoid progenitors from ES cells, which were enriched in CD34(+) CD31(lo) and CD34(+) CD45(-)cell populations, respectively, in a dose-dependent manner. Furthermore, during the 7 days of in vitro differentiation, BMP-4 was required within the first 4 days, whereas VEGF was functional after the action of BMP-4 (in the last 3 days). Thus, VEGF is a synergistic enhancer for the BMP-4-dependent differentiation processes, and it seems to be achieved by the ordered action of the 2 factors.

Antigens, CD34↗
PubMedDate not supplied

Donor leukocyte infusion--the effect of mutual reactivity of donor's and recipient's peripheral blood mononuclear cells on hematopoietic progenitor cells growth.

Donor leukocyte infusions are an effective therapy for patients who relapse with leukemia after bone marrow transplantation. We report the case of 14-year-old boy who relapsed 34 months after sibling donor bone marrow transplant for Philadelphia-positive chronic myeloid leukemia. Subsequently, he received three infusions of donor mononuclear cells (DMNC) harvested in steady state hematopoiesis and one G-CSF mobilized-peripheral blood mononuclear cells (PBMC) infusion. Simultaneously, test named as--"Test of Mixed Progenitors" (TMP) was performed for the assessment whether the outcome of donor leukocyte infusion treatment could be predicted. Prior to DMNC infusions, the CFU-GM and BFU-E colony assays were performed for donor's and recipient's PBMC individually, as well as for the mixture of these cells at 1:1 ratio. The cells were plated either directly in the semisolid medium or after 24 h preincubation treatment. Significantly lower values for CFU-GM derived colonies were determined in TMP in comparison to the CFU-GM values obtained for the recipient's cells. The reduced number of CFU-GM was determined both in TMP performed without preincubation treatment, app. 80% and after the 24 h preincubation, app. 55%. The reduced number of BFU-E derived colonies (app. 44%) was observed only related to recipient's cells and after the preincubation treatment of the cells. The patient did not develop GVHD and currently (40 months after the first infusion). He remained well in complete hematological, cytogenetic, molecular and clinical remission, which was the most direct evidence of the GVL effect. The novel in vitro TMP test in which the specific contribution of donor's leukocytes to the growth of recipient's hematopoietic precursor cell growth was determined, correlated with the clinical outcome.

Adolescent↗