Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maturation of adult human bone marrow (BM) B cells is accompanied by the sequential acquisition and loss of characteristic cell surface antigens (Loken et al., Blood 70:1316). Little is known about these changes in fetal BM B cells. In order to compare fetal with adult B cell development, we performed three-color, flow cytometric analyses of cell surface antigens, as well as nuclear TdT staining, on lymphoid cells from fetal BM. Mononuclear cells isolated from fetal BM (18-22 weeks) were stained with combinations of antibodies against CD3, CD10, CD19, CD20, CD21, CD22, CD34, CD45, PCA-1, IgM, and HLA-DR. Analysis of six separate fetal BM specimens indicated that combinations of cell surface antigens were expressed on analogous populations in fetal and adult BM. Consistent with adult BM, greater than 95% of TdT+ cells within the CD10+ population were CD34+, whereas less than 5% were CD34-. This CD10+/CD34+/TdT+ population constituted 30-40% of the total B cell compartment, compared with 10% in adults. Quantitative changes in CD45 expression on fetal BM B cells defined three clear populations, as has been observed in adults. In striking contrast to adult BM, greater than 95% of CD19+ and greater than 95% of surface IgM+ cells were CD10+, indicating that CD10 is a pan-B cell antigen in fetal BM. Virtually no mature B cells expressing CD21, CD22, or PCA-1 were detected in fetal BM. Our results indicate a preponderance of immature phenotypes exist in the fetal BM B cell compartment. These immature cells can be grouped into three distinct populations, and probably correspond to expanded populations found less frequently in adult BM. This striking increase in the earliest identifiable stages of B cell ontogeny is consistent with an active expansion of cells destined to constitute the humoral immune system during fetal development.
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PMID:Multiparameter flow cytometric analysis of human fetal bone marrow B cells. 169 9

Detailed immunophenotypic analyses of immunologically classified leukemias and lymphomas showed that CD40 displays an exquisite B-lineage specificity within the human lymphopoietic system. Notably, 82% of B-lineage chronic lymphocytic leukemias (CLLs), 82% of B-lineage hairy cell leukemias (HCLs), 86% of B-lineage non-Hodgkin's lymphomas (NHLs), and 29% of B-lineage acute lymphoblastic leukemias (ALLs) were CD40+. Quantitative analyses of the correlated expression of CD40 and other B-lineage differentiation antigens on fetal lymphoid precursor cells by multiparameter two-color/three-color flow cytometry, combined with analyses of sequential antigen expression on fluorescence-activated cell fluorescence activated cell sorter (FACS) isolated immunologically distinct fetal B-cell precursor subpopulations during in vitro proliferation and differentiation, provided evidence that the acquisition of CD40 antigen in human B-cell ontogeny occurs subsequent to the expression of CD10 and CD19 antigens but before the surface expression of CD20, CD21, CD22, CD24, and surface immunoglobulin M (sIgM). Some leukemic pro-B cells from ALL patients as well as normal pro-B cell clones from fetal livers displaying germline Ig heavy chain genes were CD40+, indicating that the acquisition of CD40 antigen likely precedes the rearrangement of Ig heavy chain genes. CD40+ FACS-sorted malignant cells from B-lineage ALL as well as B-lineage NHL patients were capable of in vitro clonogenic growth, indicating the CD40 antigen is expressed on clonogenic leukemia and lymphoma cells. This hypothesis was confirmed by the ability of an anti-CD40 immunotoxin that we used as an antigen-specific cytotoxic probe to effectively kill clonogenic B-lineage ALL and NHL cells.
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PMID:Temporal association of CD40 antigen expression with discrete stages of human B-cell ontogeny and the efficacy of anti-CD40 immunotoxins against clonogenic B-lineage acute lymphoblastic leukemia as well as B-lineage non-Hodgkin's lymphoma cells. 170 26

The lymphoid tissue of the human fetal spleen at various stages of gestation was studied on frozen and paraffin sections and with two-colour flow cytometry. On the sections scattered lymphoid cells and perivascular lymphoid aggregates were found starting from the 15th week of gestation. CD3, CD5, CD19, CD20, CD21, CD22, CD24, CD35, CD38-positive cells were observed. No CD10- and CD23-positive cells were detected. Flow cytometry showed a prevalence of B-lymphocytes. The majority of them expressed CD5 antigen. These cells were also IgM/D, CD19, CD20, CD21, CD22, CD24 and CD35-positive. Only few of them expressed CD10 and CD23. A similar phenotype was found in human cord blood. By contrast, in adult spleens CD5 B-cells never exceeded 8% of the B-cells. The comparison between CD5 B-cells of fetal spleen and CD5 B neoplastic cells of 72 cases of small B-cell lymphomas showed that CD23, which was usually expressed by a high percentage of the neoplastic cells, particularly in B-CLL, was not displayed by the majority of the CD5 non neoplastic cells. The reverse was shown by CD35. These findings suggest that different states of activation distinguish the normal CD5 B-cells from their malignant counterpart.
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PMID:CD5-positive B-cells of the fetal and adult spleen lymphoid tissue: an immunophenotypical study. 170 75

A number of markers which have been proposed to identify B cell subsets have been reassessed on human B cells, using an immunofluorescence technique optimized for sensitivity and an analytical mode which yields histograms showing the distribution of fluorescence on B cells. The results show that CD38, CD22, CD23, FMC6, and anti-IgM react with all blood B cells, albeit with a broad and complex distribution of fluorescence. CD5, CD9, CD10, CD43, and IgD can be regarded as subset markers since they give clearly bimodal distributions of fluorescence intensity. CD5 staining showed at least three populations, with a small number (3-5 per cent) of cells brightly stained and a population of variable size staining weakly. No clearly defined populations were seen with CD45R0, although staining was slightly above background. An antibody against the LAM-1 molecule reacted with all blood B cells. Expression of the IL-2 receptor p55 chain (CD25) was clearly bimodal, whereas the p75 chain was essentially negative on B cells. The relationship between subsets in blood and subsets in tissue, and between subsets identified by different markers in blood, is discussed.
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PMID:The expression of sub-population markers on B cells: a re-evaluation using high-sensitivity fluorescence flow cytometry. 172 68

Cytogenetic, biomolecular, and clinicopathologic features were retrospectively studied in 34 adult patients with acute myelogenous leukemia expressing one or more of the following lymphoid-associated markers (LMs): CD7, CD2, CD10, CD19, CD22, TdT. Six patients showed 11q23 rearrangements (group I); three patients had the classic Ph chromosome (group II); 15 patients had aberrations of the myeloid type (group III), including four patients with structural aberrations of 13q or trisomy 13, three patients with 7q and 1q anomalies, and two patients with trisomy 11q. Ten patients had a normal karyotype (group IV). Anomalies exclusively associated with lymphoid malignancies were not seen. Ig H and/or T-cell receptor genes were found to be rearranged in 50% and 66% of patients in cytogenetic groups I and II, respectively, versus 8% in group III and 12% in group IV. Likewise, more than one LM was more frequently detected in groups I and II. In group III, two of four patients with aberrations of chromosome 13 expressed two or more lymphoid features. Clinically, patients belonging to cytogenetic groups I and II were generally young, presented with a high white blood cell (WBC) count, and had a low complete remission rate. Survival in Ph chromosome-positive cases was uniformly short. We conclude that although there is no cytogenetic anomaly specifically associated with acute myelogenous leukemia expressing LM, a Morphologic, Immunologic, and Cytogenetic classification may constitute a working basis for further studies aimed at a better definition of clinicopathologic features and optimal treatment strategies for these leukemias.
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PMID:Correlation of cytogenetic patterns and clinicobiological features in adult acute myeloid leukemia expressing lymphoid markers. 151 51

In this report we describe the use of the immunomagnetic depletion of tumor cells from harvested bone marrow in two patients with acute lymphoblastic leukemia. The immunomagnetic procedure of purging involved one incubation of the marrow cells with a mixture of 4 monoclonal antibodies which bind to antigens of CD10 (ALB2), CD19 (HD37), CD20 (B1) and CD22 (HD39). Two incubations with magnetic beads (Dynabeads M-450) covered with antimouse antibodies followed by magnetic separation were performed. The bead/target B cell ratio was 50:1. After purging the recovery of mononuclear cells was 56% and 40%, while the recovery of CFU-GM was 45% and 38% respectively. Both patients engrafted rapidly without serious complications. One patient relapsed 4 months after transplant, the other remains in complete remission after 5 months. Our results confirm that the use of immunomagnetic beads is a simple, safe and reproducible technique to remove tumor cells before ABMT in patients with B malignancies using a broad mixture of MoAbs. However only a randomized trial using autologous marrow purged or not will clarify the effective clinical value of the procedure.
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PMID:Immunomagnetic purging procedure for autologous bone marrow transplantation in lymphoid malignancies. 186 52

We show here that analysis of VpreB gene transcription can be a specific way to identify acute leukemias of cells at very early stages of B-cell development. Northern blot analysis of RNAs from 63 leukemia samples showed that VpreB RNA was present in malignancies of precursor B cells, the expression being a feature of both common acute lymphoblastic leukemia (ALL) (CD10+) and null ALL (CD10-). It was absent from malignancies of mature B cells (surface Ig positive), from acute leukemias of the T-cell lineage and granulocyte-macrophage lineages, and from normal tonsil B and T lymphocytes. Chronic myeloid leukemia blast crises of the B-precursor-cell type expressed the VpreB gene while myeloid blast crises did not. VpreB RNA was also expressed in the neoplastic cells of one of three patients with acute undifferentiated leukemias. These data show that VpreB RNA expression is a marker of the malignant forms of precursor B cells, and that it appears at least as early as cytoplasmic CD22 and CD19 in tumors of the B-cell lineage.
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PMID:VpreB gene expression in hematopoietic malignancies: a lineage- and stage-restricted marker for B-cell precursor leukemias. 188 24

Human B lymphocyte differentiation is regulated by signals transmitted after binding of cytokines to their specific receptors and/or cross-linking of cell-cell adhesion receptors. In addition to surface immunoglobulin (sIg) receptors for antigen, a number of B cell-associated surface molecules have now been identified which may regulate activation and adhesion of B cells. These include members of the Ig supergene family such as CD19, CD22, B7/BB1, and BMC1, cell surface enzymes such as CD10, CD73, and CDw75, and proteins with multiple transmembrane domains such as CD20 and CD37. In this review we describe how several of these accessory molecules may affect signaling via antigen receptors and influence primary vs secondary immune responses. For instance, signaling via either CD21 or CD22 can augment responses to anti-Ig; the B cell activation marker B7/BB1 may function to trigger T cells via its ligand, CD28, to produce cytokines which in turn stimulate B cells; and the receptor, CD40, may transmit a signal to protect germinal center B cells from undergoing programmed cell death. Understanding how B cell accessory molecules regulate key interconnections during development may provide insights into the control and management of diseases with B-cell dysfunctions.
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PMID:Regulation of human B-cell activation and adhesion. 191 Jun 93

The aim of the present study was to compare the immunofluorescence technique (IF) with the immunoenzymatic (IE) alkaline phosphatase-antialkaline phosphatase method for the evaluation of the presence of lymphoid antigens (Ag) in 46 cases of acute myeloid leukemia (AML). The first technique allows detection of Ag expressed on the cytoplasmic membrane of living cells, whilst the second shows the presence of intracytoplasmic Ag on fixed cells. In general, the percentages of lymphoid Ag expression on AML cells are relatively low with both IE (15.2%) and IF (17.4%). We found a good correlation between the two methods for CD2 (4/4), CD7 (4/5), CD20 (1/1) and CD4 (2/2). The Ag CD19, CD21 and CD8 were negative in all cases, both with IE and with IF. CD3 (2 cases) and CD22 (1 case) were only evident with IE. CD10 was seen in 1 case with IF, whilst it was found more frequently with IE. For this reason, demonstration of CD10 with IF is more specific for the classification of acute leukemia.
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PMID:Incidence of lymphoid markers in acute myeloid leukemia. Alkaline phosphatase-antialkaline phosphatase versus immunofluorescence. 195 Mar 56

To compare the differentiation of early B- and T-lymphoid precursors, we have used immune adherence combined with analytical flow cytometric techniques to enrich and characterize subsets of the small population of bone marrow mononuclear cells that express the enzyme terminal deoxynucleotidyl transferase (TdT) but lack the CD19 B-lymphoid marker. Two percent to five percent of bone marrow TdT + mononuclear cells belong to the T-lymphoid lineage by virtue of expression of CD7 or CD5. Three-color immunofluorescence studies showed that, like early B-lymphoid precursors, most bone marrow TdT + T cells express HLA-DR and the progenitor cell antigen CD34, and about half express CD10. All CD5 + TdT + cells express surface CD3 and T-cell receptor alpha, beta, while a subset of CD7 + TdT + cells lack these "mature" T cell features. CD2 is low or absent on CD5 + TdT + cells. Examination of isolated CD34 + cells showed that approximately 70% of CD34 + TdT + cells expressed neither CD19, CD22, CD7, nor CD5, and 15% to 50% also lacked CD10. Thus, a major subset of CD34 + TdT + cells lack lineage-specific surface antigens. TdT expression may be the earliest available marker of lymphoid differentiation, and CD34 + TdT + cells are likely to include progenitor cells for both the B and T lineages.
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PMID:Normal human bone marrow precursors that express terminal deoxynucleotidyl transferase include T-cell precursors and possible lymphoid stem cells. 201 96


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