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Host-versus-graft disease in mice after the induction of neonatal transplantation tolerance by two different methods
1Department of Experimental Surgery, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Newborn A mice were injected either with a single i.v. dose (Group A) or with repeated doses of (B10 x A)F1 semiallogeneic spleen cells (SSC) (Group B). A similar degree of partial transplantation tolerance (TT) to B10 skin allografts was revealed in both groups. No signs of acute, rapidly fatal host-versus-graft disease (HVGD) (anemia, leukocytosis, severe thrombocytopenia, hepatic infarcts, gastrointestinal bleedings) were found, rather a chronic HVGD developed [moderate thrombocytopenia, autoimmune antithymocyte antibodies (ATA)] in both groups. The mortality due to lymphoproliferative disorders (LPD) was significantly higher in Group A. Thus, repeated perinatal injections of (B10 x A)F1 SSC into A mice did not increase the tolerogenic and the LPD-inducing effect either, and they did not elicit acute HVGD in contrast to observations in other F1 donor-recipient combinations [1]. Consequently, the development of acute HVGD depends on immunogenetic factors and not on the repeated administration of SSC.
Newborn A mice were injected either with a single i.v. dose (Group A) or with repeated doses of (B10 x A)F1 semiallogeneic spleen cells (SSC) (Group B). A similar degree of partial transplantation tolerance (TT) to B10 skin allografts was revealed in both groups. No signs of acute, rapidly fatal host-versus-graft disease (HVGD) (anemia, leukocytosis, severe thrombocytopenia, hepatic infarcts, gastrointestinal bleedings) were found, rather a chronic HVGD developed [moderate thrombocytopenia, autoimmune antithymocyte antibodies (ATA)] in both groups. The mortality due to lymphoproliferative disorders (LPD) was significantly higher in Group A. Thus, repeated perinatal injections of (B10 x A)F1 SSC into A mice did not increase the tolerogenic and the LPD-inducing effect either, and they did not elicit acute HVGD in contrast to observations in other F1 donor-recipient combinations [1]. Consequently, the development of acute HVGD depends on immunogenetic factors and not on the repeated administration of SSC.