Induction of Either Acute or Chronic Graft-Versus-Host Disease Due to Genetic Differences Among Donor T Cells
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).
KeywordsSpleen Cell Aplastic Anemia Acute GVHD Hygienic Quality Cytotoxic Index
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