scholarly journals Analysis of leukocyte differentiation antigens in blood and bone marrow from preleukemia (refractory anemia) patients using monoclonal antibodies

Blood ◽  
1986 ◽  
Vol 67 (4) ◽  
pp. 898-902
Author(s):  
P Hokland ◽  
G Kerndrup ◽  
JD Griffin ◽  
J Ellegaard
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
T Lymphocytes ◽  
Peripheral Blood ◽  
Defense Mechanisms ◽  
Mononuclear Cells ◽  
Myeloid Cells ◽  
Suppressor Cells ◽  
Refractory Anemia ◽  
Differentiation Antigens

Peripheral blood and bone marrow mononuclear cells from patients with refractory anemia (RA) or RA with sideroblasts (defined according to the revised French-American-British classification with less than 5% blast cells in the bone marrow) were analyzed using a panel of monoclonal antibodies directed against leukocyte antigens on B lymphocytes, T lymphocytes, monocytes, and myeloid cells. In the peripheral blood an increased proportion of T lymphocytes (and correspondingly a decreased proportion of B cells) could be demonstrated. However, when expressed in terms of absolute numbers, the T cell component was depressed because of severely decreased numbers of T4+ helper cells. In contrast, the absolute numbers of T8+ suppressor cells were either normal or increased in the majority of the patients. This resulted in markedly decreased ratios of T4+/T8+ cells, which were closely correlated to the number of transfusions given to the patients because of their refractory anemia. Finally, nearly all of the patients exhibited decreased numbers of cells reactive with the N901 natural killer (NK) antibody, thus explaining our earlier finding of decreased NK activity in these patients. In the bone marrow increased proportions of myeloid cells reactive with monoclonal antibodies present on immature myeloid cells (My7 and My9) were found, suggesting the presence of malignant clones. Indeed, when the numbers of My7+ cells and the morphologic evaluations of bone marrow smears at the time of diagnosis were compared to the progression of the disease, a group of patients with high numbers of My7+ cells and normal morphology could be identified that had a high probability of progression to refractory anemia with an excess of blasts or to overt acute myeloid leukemia. Thus, the use of antibodies defining leukocyte differentiation antigens might be of significant value in the diagnosis and prognostication of the myelodysplastic syndromes. These findings are discussed in relation to the pathogenesis of this potentially premalignant condition with special emphasis on possible defects in the immunologic defense mechanisms against early neoplasias.

scholarly journals Analysis of leukocyte differentiation antigens in blood and bone marrow from preleukemia (refractory anemia) patients using monoclonal antibodies

Blood ◽  
1986 ◽  
Vol 67 (4) ◽  
pp. 898-902 ◽  
Author(s):  
P Hokland ◽  
G Kerndrup ◽  
JD Griffin ◽  
J Ellegaard
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
T Lymphocytes ◽  
Peripheral Blood ◽  
Defense Mechanisms ◽  
Mononuclear Cells ◽  
Myeloid Cells ◽  
Suppressor Cells ◽  
Refractory Anemia ◽  
Differentiation Antigens

Abstract Peripheral blood and bone marrow mononuclear cells from patients with refractory anemia (RA) or RA with sideroblasts (defined according to the revised French-American-British classification with less than 5% blast cells in the bone marrow) were analyzed using a panel of monoclonal antibodies directed against leukocyte antigens on B lymphocytes, T lymphocytes, monocytes, and myeloid cells. In the peripheral blood an increased proportion of T lymphocytes (and correspondingly a decreased proportion of B cells) could be demonstrated. However, when expressed in terms of absolute numbers, the T cell component was depressed because of severely decreased numbers of T4+ helper cells. In contrast, the absolute numbers of T8+ suppressor cells were either normal or increased in the majority of the patients. This resulted in markedly decreased ratios of T4+/T8+ cells, which were closely correlated to the number of transfusions given to the patients because of their refractory anemia. Finally, nearly all of the patients exhibited decreased numbers of cells reactive with the N901 natural killer (NK) antibody, thus explaining our earlier finding of decreased NK activity in these patients. In the bone marrow increased proportions of myeloid cells reactive with monoclonal antibodies present on immature myeloid cells (My7 and My9) were found, suggesting the presence of malignant clones. Indeed, when the numbers of My7+ cells and the morphologic evaluations of bone marrow smears at the time of diagnosis were compared to the progression of the disease, a group of patients with high numbers of My7+ cells and normal morphology could be identified that had a high probability of progression to refractory anemia with an excess of blasts or to overt acute myeloid leukemia. Thus, the use of antibodies defining leukocyte differentiation antigens might be of significant value in the diagnosis and prognostication of the myelodysplastic syndromes. These findings are discussed in relation to the pathogenesis of this potentially premalignant condition with special emphasis on possible defects in the immunologic defense mechanisms against early neoplasias.

scholarly journals Characterization of the potentiation effect of activin on human erythroid colony formation in vitro

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 952-960 ◽  
Author(s):  
J Yu ◽  
L Shao ◽  
J Vaughan ◽  
W Vale ◽  
AL Yu
Keyword(s):  
Bone Marrow ◽  
T Lymphocytes ◽  
Dna Synthesis ◽  
Peripheral Blood ◽  
Colony Formation ◽  
Mononuclear Cells ◽  
Erythroid Progenitors ◽  
Potentiation Effect ◽  
Proliferation And Differentiation

Activin, also named FSH-releasing protein, was previously shown to induce hemoglobin accumulation in K562 cells and potentiate the proliferation and differentiation of CFU-E in human bone marrow cultures. Present studies indicate that the potentiation effect of activin is lineage specific. In addition to CFU-E, activin caused an increase in the colony formation of BFU-E from either bone marrow or peripheral blood. It had little effect on the colony formation of CFU- GM and the mixed colonies from CFU-GEMM. In serum-depleted culture, the effect of activin was shown to be dose-dependent with doses effective at picomolar concentrations. The potentiation effect of activin was exerted indirectly through mediation of both monocytes and T lymphocytes. Activin was also found to increase specifically the proportion of DNA-synthesizing erythroid progenitors from both bone marrow and peripheral blood. It had little effect on DNA synthesis in CFU-GM and in mitogen-stimulated lymphocytes. Addition of the monocytes or T lymphocytes to their respective depleted subpopulations of mononuclear cells reconstituted the enhancing effect of activin on the colony formation and DNA synthesis of erythroid progenitors. These results strongly suggest a specific role of activin in potentiating the proliferation and differentiation of erythroid progenitors in vitro.

Juvenile Chronic Myelogenous Leukemia: Surface Antigen Phenotyping by Monoclonal Antibodies and Cytogenetic Studies

PEDIATRICS ◽  
1986 ◽  
Vol 77 (3) ◽  
pp. 330-335
Author(s):  
Kevin Shannon ◽  
Gabriel Nunez ◽  
Lois W. Dow ◽  
Arthur G. Weinberg ◽  
Yuichi Sato ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Monoclonal Antibodies ◽  
Chronic Myelogenous Leukemia ◽  
Chromosomal Abnormality ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Bone Marrow Cells ◽  
Myelogenous Leukemia ◽  
Peripheral Blood Mononuclear

Cells from three children with juvenile chronic myelogenous leukemia were studied using culture in semisolid media, cytogenetic analysis, and surface staining with the monocyte-specific monoclonal antibodies 61D3 and 63D3. The percentage of bone marrow mononuclear cells that were 61D3- and 63D3-positive was markedly increased in all three patients. Bone marrow and peripheral blood mononuclear cells exhibited exceptionally bright immunofluorescence with these antibodies. The presence of monocyte-specific antigens on the surface of juvenile chronic myelogenous leukemia cells suggests that they are derived from a precursor with monocytic characteristics. A specific chromosomal abnormality (47, XY+21) was present in fresh bone marrow cells from one patient; in contrast, 50 metaphases from phytohemagglutinin-stimulated peripheral blood contained a normal karyotype. The chromosomal abnormality was also identified in myeloid colonies grown in vitro from this patient. Granulocytic elements were demonstrated in tissue sections and in cultured myeloid colonies from this child. Our data suggest that malignant transformation in juvenile chronic myelogenous leukemia involves a myeloid progenitor population capable of differentiation in vitro to cells with monocytic or granulocytic characteristics.

The Role of Human Leukocyte Antigen G in Inducing Immune Tolerance After Allogeneic Hematopoietic Stem Cell Transplantation.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4478-4478
Author(s):  
Xuan Du ◽  
Xiuli Wu ◽  
Rui Li ◽  
Zhiping Fan ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Lymphocytes ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Culture Supernatant ◽  
Hematopoietic Stem ◽  
Ifn Γ ◽  
High Level

Abstract Abstract 4478 Background and Objective Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is now applied widely for the treatment of hematological or non-hematological malignancies, aplastic anemia and hereditary diseases. Recently, a protocol for haploidentical allo-HSCT that combines granulocyte-colony stimulating factor (G-CSF) primed bone marrow (G-BM) and peripheral blood stem cells (G-PBSC) without in vitro T-cell depletion received great success. But the mechanism of G-CSF inducing immunotolerance in haploidentical-HSCT has not yet been clarified. Human leucocyte antigen G (HLA-G) is a nonclassical HLA class I molecule, the tolerogenic role of HLA-G is highly supported in pregnancy immunization, tumor immune escape and organ transplant. Because HLA-G closely related to immunotolerance, we investigate the role of HLA-G in inducing immune tolerance after allo-HSCT and the effects of G-CSF on the expression and secretion level of HLA-G. Methods Flow cytometry was used to detect the expression of membrane-bound HLA-G (mHLA-G) on donor peripheral blood cells (PBC) or bone marrow (BM) cells. The levels of soluble HLA-G (sHLA-G) in the plasma and bone marrow fluid were determined by enzyme-linked immunosorbent assay (ELISA). In vitro, the expression and secretion level of HLA-G in bone marrow mononuclear cells (BMMCs) and peripheral blood mononuclear cells (PBMCs) after G-CSF stimulated were detected by flow cytometry and ELISA, respectively; Separated T lymphocytes which expressed high level of HLA-G were cultured with allogeneic T lymphocytes and relative response index (RPI) was measured with MTT assay; Furthermore, separated T lymphocytes were cultured with allogeneic BMMCs and the levels of IFN-γ and IL-10 in culture supernatant were determined by ELISA. Results The mean level of mHLA-G after G-CSF mobilization in the PBC or BM cells was significantly higher than that before G-CSF mobilization (P<0.05). The level of mHLA-G or sHLA-G in BM cells was higher than that in PBC after G-CSF mobilization (P<0.05). The level of mHLA-G or sHLA-G in BMMCs or PBSCs which were stimulated by G-CSF was higher than that of the controls (P<0.05), and the level of HLA-G in BMMCs was higher than that in PBSCs. HLA-G predominant expressed in CD3+ T cells; The results of allogeneic mixed lymphocyte culture revealed that immunological function of the separated T lymphocytes which expressed high level of HLA-G was inhibited (RPI: 54.3%). The separated T lymphocytes co-cultured with allogeneic BMMCs, the levels of IFN-γ and IL-10 in culture supernatant were significantly higher than the controls (P<0.05). Conclusions HLA-G is rich in G-BM that might be interpret G-BM could induce better immunotolerance than G-PBSC. The G-CSF could regulate HLA-G expression and secretion directly. The mechanism of G-CSF inducing immunotolerance might be related to the inhibition of allogeneic T cell reactivity and the increase of IFN-γ and IL-10 secretion through HLA-G. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Binding of fluorescein-labeled anaphylatoxin C5a to human peripheral blood, spleen, and bone marrow leukocytes

Blood ◽  
1992 ◽  
Vol 79 (1) ◽  
pp. 152-160
Author(s):  
T Werfel ◽  
M Oppermann ◽  
M Schulze ◽  
G Krieger ◽  
M Weber ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Bone Marrow Cells ◽  
Human Peripheral Blood ◽  
Myeloid Cells ◽  
Lymphocyte Subpopulation ◽  
Marrow Cells

The expression of C5a receptors (C5aR) on human leukocytes was evaluated by flow cytometry using fluorescein-labeled human C5a (C5a- F). Granulocytes and CD14+ mononuclear cells (MNL) but not CD3+, CD20+, CD16+, CD56+, or CD11b+ lymphocytes in peripheral blood and spleen bound C5a-F. C5a-F binding was saturable and inhibitable by anti-C5a monoclonal antibody (MoAb) C17/5 or unlabeled C5a. During hemodialysis, which led to the generation of C5a, only granulocytes and monocytes increased their expression of the adhesion molecule CD11b (CR3). In vitro, C5a induced an increase of CR3 and p 150/95 (CD11c/CR4) only on myeloid cells. However, treatment of leukocytes with phorbol 12- myristate 13 acetate increased CR3 and CR4 expression on both myeloid cells and a lymphocyte subpopulation. Stimulation of MNL in mixed lymphocyte cultures or by treatment with conditioned medium or with IFN- gamma did not induce binding sites for C5aR on lymphocytes and reduced the binding of C5a-F to monocytes. The expression of C5aR on low- density bone marrow cells was analyzed by setting appropriate gates during flow cytometry. Cells that bound C5a-F were found in all populations that contained granulocyte and monocyte precursors, but not in lymphocyte precursor populations. All C5aR+ bone marrow cells were CD34 and expressed high levels of CR3, which suggests a late appearance of C5aR during myeloid cell maturation. Our results indicate that C5aR is exclusively expressed on myeloid cells within the hematopoetic cell population.

scholarly journals Characterization of the potentiation effect of activin on human erythroid colony formation in vitro

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 952-960 ◽  
Author(s):  
J Yu ◽  
L Shao ◽  
J Vaughan ◽  
W Vale ◽  
AL Yu
Keyword(s):  
Bone Marrow ◽  
T Lymphocytes ◽  
Dna Synthesis ◽  
Peripheral Blood ◽  
Colony Formation ◽  
Mononuclear Cells ◽  
Erythroid Progenitors ◽  
Potentiation Effect ◽  
Proliferation And Differentiation

Abstract Activin, also named FSH-releasing protein, was previously shown to induce hemoglobin accumulation in K562 cells and potentiate the proliferation and differentiation of CFU-E in human bone marrow cultures. Present studies indicate that the potentiation effect of activin is lineage specific. In addition to CFU-E, activin caused an increase in the colony formation of BFU-E from either bone marrow or peripheral blood. It had little effect on the colony formation of CFU- GM and the mixed colonies from CFU-GEMM. In serum-depleted culture, the effect of activin was shown to be dose-dependent with doses effective at picomolar concentrations. The potentiation effect of activin was exerted indirectly through mediation of both monocytes and T lymphocytes. Activin was also found to increase specifically the proportion of DNA-synthesizing erythroid progenitors from both bone marrow and peripheral blood. It had little effect on DNA synthesis in CFU-GM and in mitogen-stimulated lymphocytes. Addition of the monocytes or T lymphocytes to their respective depleted subpopulations of mononuclear cells reconstituted the enhancing effect of activin on the colony formation and DNA synthesis of erythroid progenitors. These results strongly suggest a specific role of activin in potentiating the proliferation and differentiation of erythroid progenitors in vitro.

scholarly journals Binding of fluorescein-labeled anaphylatoxin C5a to human peripheral blood, spleen, and bone marrow leukocytes

Blood ◽  
1992 ◽  
Vol 79 (1) ◽  
pp. 152-160 ◽  
Author(s):  
T Werfel ◽  
M Oppermann ◽  
M Schulze ◽  
G Krieger ◽  
M Weber ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Bone Marrow Cells ◽  
Human Peripheral Blood ◽  
Myeloid Cells ◽  
Lymphocyte Subpopulation ◽  
Marrow Cells

Abstract The expression of C5a receptors (C5aR) on human leukocytes was evaluated by flow cytometry using fluorescein-labeled human C5a (C5a- F). Granulocytes and CD14+ mononuclear cells (MNL) but not CD3+, CD20+, CD16+, CD56+, or CD11b+ lymphocytes in peripheral blood and spleen bound C5a-F. C5a-F binding was saturable and inhibitable by anti-C5a monoclonal antibody (MoAb) C17/5 or unlabeled C5a. During hemodialysis, which led to the generation of C5a, only granulocytes and monocytes increased their expression of the adhesion molecule CD11b (CR3). In vitro, C5a induced an increase of CR3 and p 150/95 (CD11c/CR4) only on myeloid cells. However, treatment of leukocytes with phorbol 12- myristate 13 acetate increased CR3 and CR4 expression on both myeloid cells and a lymphocyte subpopulation. Stimulation of MNL in mixed lymphocyte cultures or by treatment with conditioned medium or with IFN- gamma did not induce binding sites for C5aR on lymphocytes and reduced the binding of C5a-F to monocytes. The expression of C5aR on low- density bone marrow cells was analyzed by setting appropriate gates during flow cytometry. Cells that bound C5a-F were found in all populations that contained granulocyte and monocyte precursors, but not in lymphocyte precursor populations. All C5aR+ bone marrow cells were CD34 and expressed high levels of CR3, which suggests a late appearance of C5aR during myeloid cell maturation. Our results indicate that C5aR is exclusively expressed on myeloid cells within the hematopoetic cell population.

scholarly journals Clinical observations of bone marrow transfusion for promoting bone marrow reconstruction after chemotherapy for AIDS-related lymphoma

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yixuan Liu ◽  
Suhong Xie ◽  
Lei Li ◽  
Yanhui Si ◽  
Weiwei Zhang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Immune System ◽  
T Lymphocytes ◽  
Peripheral Blood ◽  
Autologous Bone Marrow ◽  
Control Group ◽  
Peripheral Vein ◽  
Significant Difference ◽  
Autologous Bone ◽  
Aids Related Lymphoma

Abstract Background This study investigates the effect of autologous bone marrow transfusion (BMT) on the reconstruction of both bone marrow and the immune system in patients with AIDS-related lymphoma (ARL). Methods A total of 32 patients with ARL participated in this study. Among them, 16 participants were treated with conventional surgery and chemotherapy (control group) and the remaining 16 patients were treated with chemotherapy followed by autologous bone marrow transfusion via a mesenteric vein (8 patients, ABM-MVI group) or a peripheral vein (8 patients, ABM-PI group). Subsequently, peripheral blood and lymphocyte data subsets were detected and documented in all patients. Results Before chemotherapy, no significant difference in indicators was observed between three groups of ARL patients. Unexpectedly, 2 weeks after the end of 6 courses of chemotherapy, the ABM-MVI group, and the ABM-PI group yielded an increased level of CD8+T lymphocytes, white blood cells (WBC), and platelet (PLT) in peripheral blood in comparison to the control group. Notably, the number of CD4+T lymphocytes in the ABM-PI group was significantly higher than that in the other two groups. Additionally, no significant difference in haemoglobin levels was observed before and after chemotherapy in both the ABM-MVI and ABM-PI groups, while haemoglobin levels in the control group decreased significantly following chemotherapy. Conclusions Autologous bone marrow transfusion after chemotherapy can promote the reconstruction of both bone marrow and the immune system. There was no significant difference in bone marrow recovery and reconstruction between the mesenteric vein transfusion group and the peripheral vein transfusion group.

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