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).
Supported by grants from the Queen Wilhelmina Fund for the Fight against Cancer, Amsterdam, The Netherlands, and the Volkswagen Foundation, Hannover, West Germany.
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Pals, S.T., Radaszkiewicz, T., Gleichmann, E. (1982). Induction of Either Acute or Chronic Graft-Versus-Host Disease Due to Genetic Differences Among Donor T Cells. In: Nieuwenhuis, P., van den Broek, A.A., Hanna, M.G. (eds) In Vivo Immunology. Advances in Experimental Medicine and Biology, vol 149. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-9066-4_75
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