Sequential loss of CD34 and class II MHC antigens on purified cord blood hematopoietic progenitors cultured with IL-3: characterization of CD34-, HLA-DR+ cells

Caux, Christophe; Favre, Catherine; Saeland, Sem; Duvert, V; Mannoni, P; Durand, Isabelle; Aubry, JP; Vries, JE de

doi:10.1182/blood.v74.4.1287.1287

Cited by 62 publications

(7 citation statements)

References 30 publications

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“…A decreased intensity of CD34 staining per se has been associated with maturation of the progenitor cell population (Caux et al, 1989;Sutherland et al, 1989;Okumura et al, 1992). This has been explained by a decrease in the number of CD34 molecules on individual cells.…”

Section: Discussionmentioning

confidence: 99%

Differences in the distribution of CD34 epitopes on normal haemopoietic progenitor cells and leukaemic blast cells

et al. 1996

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The CD34 molecule expressed on haemopoietic progenitor cells contains a large number of epitopes whose expression may be related to the maturation or function of the cells. Monoclonal antibodies specific for different epitopes have been reported to detect different numbers of CD34+ leukaemic blast cells. We wanted to confirm this observation and study whether parallel findings could be observed for normal haemopoietic progenitor cells. The cells were immunophenotyped by flow cytometry with a series of monoclonal antibodies reactive with different CD34 epitopes. Class III epitopes (resistant to enzymatic cleavage with neuraminidase, chymopapain and a glycoprotease from Pasteurella haemolytica) showed a broader distribution on normal haemopoietic progenitor cells and leukaemic blast cells than class I epitopes (sensitive to cleavage with all three enzymes) and class II epitopes (sensitive to degradation with glycoprotease and chymopapain, and resistant to neuraminidase). The subpopulation of normal progenitor cells which exclusively expressed class III epitopes had flow cytometric characteristics compatible with mature myeloid progenitor cells whereas class I, II and III epitopes were equally expressed on cells enriched for immature subsets. No discordant epitope expression could be observed for the more immature leukaemias (AML-M0/1) and a higher percentage of the more mature leukaemic blast cells (AML-M3 and AML-M4/5) expressed class III epitopes compared to the percentage expressing class I and II epitopes. These data indicate that CD34 class III epitopes are more broadly distributed on normal haemopoietic progenitor cells and leukaemic blast cells than class I and II epitopes, and that class I and II epitopes may be down-regulated prior to class III epitopes during normal haemopoietic progenitor cell differentiation. These findings should be considered when selecting CD34 mabs for quantification and positive selection of haemopoietic progenitor cells for research and clinical purposes.

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Section: Discussionmentioning

confidence: 99%

Differences in the distribution of CD34 epitopes on normal haemopoietic progenitor cells and leukaemic blast cells

et al. 1996

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“…CD34 is a highly glycosylated transmembrane protein, a member of the sialomucin family of surface antigens. CD34 is strongly expressed on hematopoietic stem/progenitor cells (HSCs), and its expression shows a progressive and rapid decline as HSCs undergo differentiation [1]. Since its discovery, CD34 has become the most widely used marker for the enrichment of human hematopoietic progenitors, but despite its importance, its function and regulation are not completely understood [2].…”

Section: Introductionmentioning

confidence: 99%

Role of CD34 Antigen in Myeloid Differentiation of Human Hematopoietic Progenitor Cells

et al. 2008

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CD34 is a transmembrane protein that is strongly expressed on hematopoietic stem/progenitor cells (HSCs); despite its importance as a marker of HSCs, its function is still poorly understood, although a role in cell adhesion has been demonstrated. To characterize the function of CD34 antigen on human HSCs, we examined, by both inhibition and overexpression, the role of CD34 in the regulation of HSC lineage differentiation. Our results demonstrate that CD34 silencing enhances HSC granulocyte and megakaryocyte differentiation and reduces erythroid maturation. In agreement with these results, the gene expression profile of these cells reveals the upregulation of genes involved in granulocyte and megakaryocyte differentiation and the downregulation of erythroid genes. Consistently, retroviral-mediated CD34 overexpression leads to a remarkable increase in erythroid progenitors and a dramatic decrease in granulocyte progenitors, as evaluated by clonogenic assay. Together, these data indicate that the CD34 molecule promotes the differentiation of CD34؉ hematopoietic progenitors toward the erythroid lineage, which is achieved, at least in part, at the expense of granulocyte and megakaryocyte lineages. STEM CELLS 2008;26:950 -959 Disclosure of potential conflicts of interest is found at the end of this article.

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“…We strongly support the hypothesis that a simultaneous increase in TNF-a production by BM lymphocytes and sensitivity of stem cells to TNF-a leads to BM failure in AA. obtain further information about the role of lymphocytes, as it is possible to analyze levels of cytokines in different lymphocyte subpopulations (16)(17)(18). We measured levels of T-cell derived intracellular cytokine production by T cells in BM of patients with AA.…”

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confidence: 99%

Excessive production of tumor necrosis factor‐alpha by bone marrow T lymphocytes is essential in causing bone marrow failure in patients with aplastic anemia

Hara

Ando

Tsurumi

et al. 2004

European J of Haematology

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Aplastic anemia (AA) is regarded as an immunological disorder because of the clinical effect of immunosuppressive therapy. Recent studies have reported that cytokines play an important role in the development of AA. In the present study, we measured levels of T-cell derived intracellular cytokine production in peripheral blood and bone marrow (BM) of patients with AA. We demonstrated that BM lymphocytes, particularly CD4(+) and CD8(+) T cells, in patients with AA produced significantly higher amounts of tumor necrosis factor-alpha (TNF-alpha), compared with lymphocytes in normal controls. We have previously reported that expression of TNF receptor (R)1 and TNFR2 in the CD34(+) CD38(-) and CD34(+) CD38(+) fractions of patients with AA is significantly higher than those in normal control. These results indicate that BM stem cells in patients with AA may possess high sensitivity to TNF-alpha. This in turn suggests that TNF-alpha affects hematopoiesis at an earlier stage in AA patients than in normal controls. We strongly support the hypothesis that a simultaneous increase in TNF-alpha production by BM lymphocytes and sensitivity of stem cells to TNF-alpha leads to BM failure in AA.

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Sequential loss of CD34 and class II MHC antigens on purified cord blood hematopoietic progenitors cultured with IL-3: characterization of CD34-, HLA-DR+ cells

Cited by 62 publications

References 30 publications

Differences in the distribution of CD34 epitopes on normal haemopoietic progenitor cells and leukaemic blast cells

Differences in the distribution of CD34 epitopes on normal haemopoietic progenitor cells and leukaemic blast cells

Role of CD34 Antigen in Myeloid Differentiation of Human Hematopoietic Progenitor Cells

Excessive production of tumor necrosis factor‐alpha by bone marrow T lymphocytes is essential in causing bone marrow failure in patients with aplastic anemia

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