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)

We investigated the expression of CD44 molecule on CD34+ hematopoietic progenitor cells. Significantly lower expression of CD44 was observed on bone marrow (BM) CD34+ cells compared with circulating CD34+ cells in cord blood and peripheral blood. Using fluorescence-activated cell sorting, human CD34+ BM cells were fractionated into CD44+ and CD44- populations. Immunofluorescence analysis revealed that the majority of CD34+CD44- cells expressed B-lymphocyte-associated CD10 and CD19 antigens, whereas only a part of CD34+CD44+ cells were positive for CD19. Myeloid and erythroid progenitor cells were found predominantly in CD34+ CD44+ cell fractions. In short-term suspension cultures, cell proliferation and G1-->S transition in the cell cycle were enhanced in CD34+CD44+ cells. In contrast, a large part of CD34+CD44- cells underwent apoptotic cell death. Although co-culture with BM stromal cells could partially prevent CD34+CD44- cells from undergoing apoptosis, significant increase of apoptotic cells was consistently observed. Furthermore, CD34+CD44- cells plated on BM stromal cells could differentiate into CD34-CD44-CD10-CD19+ cells. These findings suggest that CD34+CD44- cells expressing CD19 would represent unique B-lymphocyte-committed precursors in BM, which might undergo apoptotic cell death in the early steps of B-cell differentiation.
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PMID:Expression of homing-associated cell adhesion molecule (H-CAM/CD44) on human CD34+ hematopoietic progenitor cells. 1008 18

We recently investigated samples of pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and normal bone marrow (BM). We found that leukemic blasts, compared to their physiologic counterpart cells, frequently display aberrant phenotypes with respect to levels of expression of certain antigens. Using multiparameter flow cytometry, these differences enabled us to trace leukemic cells admixed to normal BM, which suggested that this approach might be a useful strategy for minimal residual disease detection. In the present study, we used the same multiparameter approach ("comparative phenotype mapping") to prove that such quantitative phenotypic differences really exist between malignant and normal BCP when simultaneously present in the BM. We demonstrate this by five exemplary follow-up BM samples from patients with BCP-ALL, all of which showed phenotypically aberrant cells according to levels of expression of CD10, CD11a, CD19, CD34, CD44, or CD45RA, as well as according to altered orthogonal light scattering properties. We confirmed the leukemic nature of these cells by polymerase chain reaction-based detection of bcr1/abl transcripts, and of leukemia clone-specific immunoglobulin heavy chain rearrangements in only the suspicious cells when sorted by flow cytometry, but not in normal BCP or non-B cells. Comparative phenotype mapping thus allows one to distinguish between normal and leukemic cells, and we show that it may enable rapid, specific, and quantitative detection of residual/resurgent leukemia in BCP-ALL.
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PMID:Detection of residual disease in pediatric B-cell precursor acute lymphoblastic leukemia by comparative phenotype mapping: a study of five cases controlled by genetic methods. 1021 Mar 25

Recirculation of B lymphocytes through the secondary lymphoid organs is key for recognition and response to foreign antigen. B lymphocytes within secondary lymphoid organs comprise a heterogeneous population of cells at distinct differentiation stages. To ascribe a particular adhesive behavior to discrete B-cell subsets within secondary lymphoid organs, we investigated their functional interaction with endothelial selectins under flow. We describe herein the characterization of a subset of human tonsillar B cells that interact with E-selectin but not P-selectin. E-selectin-interacting B cells had a phenotype of non-germinal center (CD10(-), CD38(-), CD44(+)), memory (IgD-) cells. Furthermore, FucT-VII was expressed selectively in CD44(+) E-selectin-adherent B lymphocytes. B-cell rolling on E-selectin required sialic acid but was independent of previously described selectin ligands. A novel glycoprotein ligand of 240 kDa carrying N-linked glycans was isolated from B-cell membranes by an E-selectin immunoadhesin. Binding of this protein was strictly Ca2+ dependent, was inhibited by a cell adhesion-blocking mAb against E-selectin, and required the presence of sialic acid but not N-linked carbohydrates. Our results enable us to assign to resident memory B lymphocytes a novel adhesion function, the rolling on E-selectin, that provides insights on the adhesion pathways involved in homing of memory B cells to tertiary sites.
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PMID:Memory B lymphocytes from secondary lymphoid organs interact with E-selectin through a novel glycoprotein ligand. 1022 75

The precise signaling pathways to induce a germinal center (GC) phenotype and somatic mutations in human B cells are presently not understood. Major phenotypical hallmarks of a human GC B cell are up-regulated expression of CD10 and CD95 together with a heterogeneous expression of CD77. Activation of resting human tonsillar B cells using anti-CD40 and anti-IgM antibodies normally only induces up-regulation of CD38 and CD71 but has no effect on the typical GC markers. However, we show here that an additional co-ligation of the glycoprotein CD44 on such tonsillar B cells up-regulated the typical human GC markers CD10, CD38, CD77 and CD95, and down-regulated CD24 and CD39 as well as induced progression towards apoptosis in these cells; all characteristics of GC B cells. These data indicate a functional role of CD44 during activation of human naive B lymphocytes and in the generation of GC B cells.
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PMID:Co-ligation of CD44 on naive human tonsillar B cells induces progression towards a germinal center phenotype. 1033 Feb 79

We developed a murine IgG1 mAb, 5G9, following immunization of a BALB/c mouse with Daudi cells. By immunoprecipitation, 5G9 reacted with a 220-kDa Ag on Daudi cells, which reduced to four subunits (55, 65, 80, and 85 kDa). mAb 5G9 bound to 40-60% of peripheral blood B cells, weakly reacted with monocytes and granulocytes, and did not bind to erythrocytes, platelets, T cells, or NK cells. mAb 5G9 brightly stained scattered cells in human tonsil sections, which appeared to be dendritic cells (DC) by morphology. mAb 5G9 also stained scattered cells in cytospin slides of monocyte-derived DC with long, thin, beaded membrane processes, morphologically distinct from other monocyte-derived DC. Positive selection of blood mononuclear cells with mAb 5G9 and sheep anti-mouse IgG Dynabeads demonstrated an enriched population of DC. By flow cytometry analysis, these cells were CD19, CD20, CD22, CD40, CD44, CD83, CD86, IgD, and HLA-Dr positive and either kappa- or lambda-L chain positive. They did not express CD3, CD4, CD5, CD10, CD11b, CD13, CD25, CD56, CD14, CD33, or CD64. Isolated 5G9+ cells were potent APCs in allogeneic MLR, compared with 5G9- PBMC, 5G9- B cells, monocytes, and monocytes cultured in IL-4 and GM-CSF for 24 h. mAb 5G9 defines a novel peripheral blood cell with B cell phenotype and DC morphology and function: DC-like B cells. The significance of this cell in immune responses requires further study.
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PMID:Human blood dendritic cell-like B cells isolated by the 5G9 monoclonal antibody reactive with a novel 220-kDa antigen. 1041 35

The nonobese diabetic/severe combined immunodeficient (NOD/SCID) xenotransplantation model is increasingly utilized to study both human lymphohematopoietic stem/progenitor cells and committed cell types. Human B lymphoid cells develop and proliferate in this model. We found high numbers of CD19+CD5+ B lymphoid cells in the bone marrows and spleens of NOD/SCID mice transplanted with human CD34+ stem/progenitor cells. The CD5+ cells accounted for a particularly large percentage of the B lymphoid cells in the spleens of chimeras analyzed three months after transplantation. CD19+CD5+ cells from all the analyzed chimeras coexpressed HLA-DR, surface IgM, CD20, CD38, CD43, and CD45. However, CD19+CD5+ cells were negative for kappa light chain, CD10, CD11a, CD11b, CD15, CD21, CD22, CD23, CD25, CD34, CD35, CD44, CD62L, CD69, and CD71. Cell surface expression of the lambda light chain, surface IgD, CD9, and CD40 antigens was detected in some but not all chimeras. Thus, the CD19+CD5+ cell population detected in our study has the phenotype of previously described CD5+ B lymphoid cells in humans and other species. The origin and role of the B lymphoid cells which express CD5 cell surface glycoprotein are poorly understood. The malignant cells in B lymphoid chronic lymphocytic leukemia express CD5, and the numbers of CD5+ B lymphoid cells are elevated in several autoimmune conditions. The human-NOD/SCID chimera system may provide an in vivo model to investigate the maturation and development of this cryptic human CD5+ B lymphoid cell subpopulation.
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PMID:Human hematopoietic stem/progenitor cells generate CD5+ B lymphoid cells in NOD/SCID mice. 1052 59

The Revised European-American Lymphoma classification gives Burkitt-like lymphoma (BLL) provisional status, leaving unresolved the differential diagnosis with Burkitt lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL). This study compared the biologic features of adult BLL and DLBCL. The phenotypic distinction between BLL and DLBCL was determined by immunohistochemical staining of frozen tissue from 13 patients with BLL and 55 patients with DLBCL by using an extensive antibody panel including Ki-67, CD10, CD11a/lymphocyte function-associated antigen 1alpha (LFA-1alpha), CD18/LFA-1beta, CD58/LFA-3, and CD54/intercellular adhesion molecule, CD8 for tumor-infiltrating cytotoxic T cells (T-TILs), CD44 homing receptor, and p53 and Bcl-2 oncogenic proteins. Compared with DLBCL, BLL had a higher proliferative rate (mean Ki-67, 88% versus 53%), greater expression of CD10 and p53 antigens, and decreased expression of Bcl-2. BLL cases had a consistent absence of one or more cell adhesion molecules (92% versus 27%), low T-TIL numbers, and absence of CD44 homing receptor (92% versus 14%). The t(8;14) translocation was identified in 80% of BLL cases, but no patients with BLL had the t(14;18) translocation. In a 10-year analysis, median survival of patients with BLL was 1.2 years, and that of patients with DLBCL was 2.5 years. Although the proportion of patients cured was similar in the 2 groups, BLL patients had an increased risk of early death. We conclude that BLL can be recognized by its combined morphologic and phenotypic features and that it represents a high-grade lymphoma much closer to BL than DLBCL. Retention of the BLL category or inclusion of BLL as a variant of BL is biologically and clinically more appropriate than absorbing the category of BLL into DLBCL. (Blood. 2001;97:3713-3720)
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PMID:The Burkitt-like lymphomas: a Southwest Oncology Group study delineating phenotypic, genotypic, and clinical features. 1138 7

Human CD34+ hematopoietic progenitor cells (HPCs) express CD44 and can directly adhere to hyaluronate (HA) via CD44. Furthermore, CD44 may also be involved in the regulation of CD34+ HPC proliferation and development. The expression of CD44 molecules on CD34+ hematopoietic progenitor cells is significantly lower on bone marrow (BM) CD34+ cells compared with circulating CD34+ cells in cord blood and peripheral blood. Myeloid and erythroid progenitor cells are found predominantly in CD34+ CD44+ cell fractions. More interestingly, CD34+ CD44- cells expressing B-lymphocyte-associated CD10 and CD19 would represent unique B-lymphocyte committed precursors in the BM, which might undergo apoptotic cell death in the early steps of B-cell differentiation.
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PMID:Homing-associated cell adhesion molecule (H-CAM/CD44) on human CD34+ hematopoietic progenitor cells. 1142 26

B lymphocytes that infiltrate the thyroid (Thy-B cells) in Graves' patients appear to be implicated in the pathophysiology of this disorder. The goal of the present study was to examine the nature of these Thy-B cells. To this end, Thy-B lymphocytes were isolated from surgical thyroidal samples, and their phenotype was determined by using mouse monoclonal antibodies (mAb) directed against a wide variety of surface markers, followed by flow cytometry multicolor analysis. The results show that most Thy-B cells (approximately 60%) exhibited IgM(+) IgD(low to -) surface immunoglobulin (Ig) profile, whereas the minor cell fraction (approximately 30%) consisted of switched IgG(+) memory B lymphocytes. Thy-B cells expressed low levels of CD5, CD23, and CD62L, which distinguished them from the resting B-cell pool, the major B-cell subset in the blood. In addition, they lacked CD38, CD10, and CD71, characteristic molecules for the germinal center B lymphocytes. In addition, Thy-B lymphocytes showed peculiar patterns both of adhesion molecules (CD62L(-), CD44(intermediate)), and of activation molecules (CD69(+), CD80(+), and, in part, CD95(+)). Taken together, these results suggest that the Thy-B lymphocyte subset consists of a combination of IgM(+) B cells resembling marginal zone B lymphocytes, and isotype-switched memory B cells.
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PMID:Thyroid-infiltrating B lymphocytes in Graves' disease are related to marginal zone and memory B cell compartments. 1144 98

CD44 expression and other B cell markers were analyzed in 38 samples of B cell precursors (BCP) from patients with acute lymphoblastic leukemia (ALL). According to the expression of CD10 and CD44, we established the following five stages of BCP-ALL phenotypes that may represent different forms of interaction between BCP-ALL and bone marrow-adherent cells: stage 1, CD19+, CD44bright, CD10-; stage 2, CD19+, CD44bright, CD10dim/bright; stage 3, CD19+, CD44dim, CD10bright, CD20-/+; stage 4, CD19+, CD44dim, CD10dim, CD20+; and stage 5, CD19+, CD44bright, CD10-, CD20+. Next, we analyzed the modulation of CD44 according to the expression of the different BCP-ALL phenotypes by incubating the samples under different culture conditions, including addition of stromal cells and interleukin (IL)-7. In culture, the samples in stages 1 and 2 maintained high expression of CD44 and re-expressed this molecule when cultured after trypsin treatment, indicating ongoing synthesis of CD44. Similarly, the stage 3 samples cultured in the presence of stromal cells, IL-7, or both also upregulated CD44 expression in culture. In contrast, the low expression of CD44 on the presumably more mature stage 4 samples was not modified by the addition of stromal cells or IL-7 or when cultured after trypsin treatment, suggesting that those cells had arrested CD44 synthesis. We concluded that down-modulation of CD44 occurred in association with differentiation to phenotype stages 3 and 4 and we hypothesized that this down-modulation might be associated with the exit of BCP-ALL from the bone marrow.
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PMID:Modulation of CD44 in acute lymphoblastic leukemia identifies functional and phenotypic differences of human B cell precursors. 1148 36


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