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Interpretations of Culture Data in Aplastic Anemia: Evidence for a Suppressor Cell Involvement

  • M. A. S. Moore
Part of the Haematology and Blood Transfusion / Hämatologie und Bluttransfusion book series (HAEMATOLOGY, volume 24)

Abstract

Aplastic anemia is a syndrome characterized by marrow hypoplasia and severe pancytopenia. While most cases of aplastic anemia have been attributed to congenital or acquired stem cell defects, it seems likely that several diseases of different etiology and pathogenesis exist. The availability of in vitro techniques for detection of myeloid and erythroid progenitor cells has provided an experimental approach for determining the mechanisms leading to aplastic anemia. Using these systems, evidence has been obtained for a reversible immunologically-mediated suppression of hematopoiesis in certain cases of aplastic anemia [1, 8]. In these studies, the severe defect in myeloid colony formation in vitro was corrected by removal of small lymphocytes from the patients’ marrow by velocity sedimentation or treatment with anti-thymocyte globulin and complement. These candidate suppressor cells were also identified by their ability to inhibit normal CFU-c when marrow from the patient was co-cultured with marrow from a normal donor in the CFU-c assay. These preliminary studies on immunologic mechanisms leading to aplasia have been confirmed by others [5, 6] and extended to a demonstration of suppression of erythroid colony formation by aplastic peripheral blood mononuclear cells.

Keywords

Aplastic Anemia Velocity Sedimentation Suppressor Cell Erythroid Progenitor Cell Colony Stimulate Activity 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Ascensao, J., Pahwa, R., Kagan, W. A., Hansen, J. A., Moore, M. A. S. and Good, R. A.: Aplastic anemia: evidence for an immunologic mechanism. Lancet I, 669–671 (1976)CrossRefGoogle Scholar
  2. 2.
    Broxmeyer, H. E., Jacobsen, N., Kurland, J., Mendelsohn, N. and Moore, M. A. S.: In vitro suppression of normal granulocyte stem cells by inhibitory activity derived from leukemic cells. J. Natl. Cancer Inst. 60, 497–511 (1978)PubMedGoogle Scholar
  3. 3.
    Broxmeyer, H. E., Smithyman, A., Eger, R. R., Meyers, P. A. and de Sousa, M.: Identification of lactoferrin as the granulocyte-derived inhibitor of colony stimulating activity (CSA)-production. J. Exp. Med. 148, 1052–1067 (1978)PubMedCrossRefGoogle Scholar
  4. 4.
    Broxmeyer, H. E., Pahwa, R., Jacobsen, N., Grossbard, E., Pahwa, S., Meyers, P. A., Kapoor, N., Miller, D., Good, R. A. Ralph, P. and Moore, M. A. S.: In vitro inhibitory activity obtained from cells of patients with neutropenias of varying etiology, (submitted)Google Scholar
  5. 5.
    Haak, H. L. and Goselink, H. M.: Mechanisms in aplastic anemia. Lancet I, 194 (1977)CrossRefGoogle Scholar
  6. 6.
    Hoffman, R., Zanjani, E. D., Lutton, J. D., Zalusky, R. and Wasserman, L. R.: Suppression of erythroid-colony formation by lymphocytes from patients with aplastic anemia. New. Eng. J. Med. 296, 10–13 (1977)PubMedCrossRefGoogle Scholar
  7. 7.
    Iscove, N., Sieber, F. and Winterhalter, K.: Erythroid colony formation in cultures of mouse and human bone marrow: Analysis of the requirement for erythropoietin by gel filtration and affinity chromatography on agarose-Con A. J. Cell. Physiol. 83, 309–320 (1974)PubMedCrossRefGoogle Scholar
  8. 8.
    Kagan, W. A., Ascensao, J. A., Pahwa, R. J., Hansen, J. A., Goldstein, G., Valera, E. B., Incefy, G. S., Moore, M. A. S. and Good, R. A.: Aplastic anemia: Presence in human bone marrow of cells that suppress myelopoiesis. Proc. Natl. Acad. Sci. (USA) 73, 2890–2894 (1976)CrossRefGoogle Scholar
  9. 9.
    Kurland, J. I., Broxmeyer, H. E., Peius, L. M., Bockman, R. S. and Moore, M. A. S.: Role for monocyte-macrophage-derived colony stimulating factor and prostaglandin E in the positive and negative feedback control of myeloid stem cell proliferation. Blood 52, 388–407 (1978)PubMedGoogle Scholar
  10. 10.
    Miller, R. and Phillips, R.: Separation of cells by velocity sedimentation. J. Cell. Physiol. 73, 191–201 (1969)PubMedCrossRefGoogle Scholar
  11. 11.
    Moore, M. A. S.: In vitro Studies in the Myeloid Leukaemias. In: Advances in Acute Leukaemia. Cleton, F. J., Crowther, D. and Malpas, J. S. (eds.). Amsterdam: ASP-Biological and Medical Press, 1974, p. 161–183Google Scholar
  12. 12.
    Moore, M. A. S.: Marrow culture — A new approach to classification of leukemias, Blood Cells 1, 149–156 (1975)Google Scholar
  13. 13.
    Singer, J. W., Brown, J. E., James, M. C., Doney, K., Warren, R. P., Storb, R. and Thomas, E. D.: The effect of peripheral blood lymphocytes from patients with aplastic anemia on granulocytic colony growth from HLA matched and mismatched marrows: The effect of transfusion sensitization. Blood (in press)Google Scholar
  14. 14.
    Thomas, E. D., Storb, R. and Giblett, E. R.: Recovery from aplastic anemia following attempted marrow transplantation. Exp. Hemat. 4, 97–102 (1976)PubMedGoogle Scholar
  15. 15.
    Torok-Storb, B. J., Storb, R., Graham, T. C., Prentice, R. L., Weiden, P. L. and Adamson, J. W.: In vitro erythropoiesis: The effect of normal versus “transfusion-sensitized” mononuclear cells. Blood 52, 607–611 (1978)Google Scholar

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© Springer-Verlag Berlin Heidelberg 1979

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  • M. A. S. Moore

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