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Induction of Either Acute or Chronic Graft-Versus-Host Disease Due to Genetic Differences Among Donor T Cells

  • S. T. Pals
  • T. Radaszkiewicz
  • E. Gleichmann
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 149)

Abstract

The clinical and pathological alterations induced by GVHR vary from stimulatory phenomena, such as SLE-like autoantibody formation, hypergammaglobulinemia, and lymphoproliferation, to suppressive phenomena, such as cellular depletion of the lympho-hemopoietic tissue accompanied by hypogammaglobulinemia and aplastic anemia. It has been established that alloreactive donor T cells are responsible for the induction of both kinds of GVH phenomena (1–5). Often during the course of acute GVHR, the lymphoid hypoplasia which eventually develops is preceded by a phase of hyperplasia. Our working hypothesis is that differences in the reactivity of allohelper and allosuppressor donor T cells account for this variability and changing nature of GVHR-induced phenomena (2). To test this hypothesis two experimental systems have been studied, which both employ adult non-irradiated (C57BL/10 × DBA/2)F1 (BDF1) mice as recipients. In one system, the different GVHR-inducing effects of two different T-cell subsets prepared from strain C57BL/10 were compared (6). In the second system (7), BDF1 mice were injected with unseparated lymphoid cells from either strain C57BL/10, B10.D2 or DBA/2. Both BIO strains were found to be potent inducers of lethal GVHD (LGVHD).

Keywords

Spleen Cell Aplastic Anemia Acute GVHD Hygienic Quality Cytotoxic Index 
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.
    E. Gleichmann, H. Gleichmann, and W. Wilke. Transplant. Rev. 31:156 (1976).PubMedGoogle Scholar
  2. 2.
    E. Gleichmann, and H. Gleichmann, in: “Immunoregulation and Autoimmunity”, p. 73, R.S. Krakauer, and M.K. Cathcart, eds., Elsevier North Holland, Inc. (1980).Google Scholar
  3. 3.
    E.H. van Elven, J. Agterberg, S. Sadal, and E. Gleichmann. J. Immunol. 126:1684 (1981).PubMedGoogle Scholar
  4. 4.
    J.P.W. van der Veen, A.G. Rolink, and E. Gleichmann. J. Immunol. (1981) in press.Google Scholar
  5. 5.
    R. Korngold, and J. Sprent. J. Exp. Med. 148:1687 (1978).PubMedCrossRefGoogle Scholar
  6. 6.
    T. Radaszkiewicz, A.G. Rolink, and E. Gleichmann. (Abstract) This volume.Google Scholar
  7. 7.
    E.H. van Elven, A.G. Rolink, F. van der Veen, and E. Gleichmann. J. Exp. Med. 153:1474 (1981).PubMedCrossRefGoogle Scholar
  8. 8.
    E. Gronowicz, A. Coutinho, and F. Melchers. Eur. J. Immunol. 6:588 (1976).PubMedCrossRefGoogle Scholar
  9. 9.
    A. van Oudenaren, H. Hooijkaas, and R. Benner. J. Immunol. Methods 43:219 (1981).PubMedCrossRefGoogle Scholar
  10. 10.
    F. van der Veen, A.G. Rolink, and E. Gleichmann. This volume.Google Scholar
  11. 11.
    K. Pickel, and M.K. Hoffmann. J. Exp. Med. 145:1169 (1977).PubMedCrossRefGoogle Scholar
  12. 12.
    D.W. van Bekkum, J. Roodenburg, P.J. Heidt, and D. van der Waay. J. Natl. Canc. Inst. 52:401 (1974).Google Scholar
  13. 13.
    Th.G. Wegmann, J. Rosovsky, G.A. Carlson, E. Diener, and D.W. Drell. J. Immunol. 125:1751 (1980).PubMedGoogle Scholar
  14. 14.
    F.L. Shand. Eur. J. Immunol. 7:746 (1977).PubMedCrossRefGoogle Scholar
  15. 15.
    F.L. Shand. Immunology 29:953 (1978).Google Scholar
  16. 16.
    H. Cantor, R.K. Gershon. Fed. Proc. 38:2058 (1979).PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • S. T. Pals
    • 1
  • T. Radaszkiewicz
    • 1
  • E. Gleichmann
    • 1
  1. 1.Central Laboratory of the Netherlands Red Cross Blood Transfusion Service and Laboratory of Experimental and Clinical Immunology of the University of AmsterdamAmsterdamThe Netherlands

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