Evaluation of Adoptive Immunotherapy for Ehrlich Tumors in Mice

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Although the genetic relationship between donor and recipient is quite critical for obtaining real effectiveness in adoptive immune transfer against cancer, the essential prerequisite in their genetic correspondence is not completely understood. For an analysis, a combination of Ehrlich ascites tumor (EAT) and mouse strains as host comprises a desirable experimental system because some mouse strains are susceptible to EAT while others are resistant. In the present series of experiments, adoptive immunotherapeutic effects on EAT were examined in mice by transferring spleen cells from EAT-regressive mouse strains to EAT-progressive ones, with the following results obtained. Activated spleen cells from B6 (H-2^b) and its Ly congenic mice such as B6-Ly-1^a, B6-Ly-2^a, and B6-Ly-2^a, 3^a as donors were very effective in suppressing EAT outgrowth in B6-nu/nu mice. No graft versus host disease (GVHD) was observed in the recipient. Activated spleen cells from other B6 congenic mice such as B6-Tla^a (H-2K^k・D^b) and B6. C-H2^<bm12> (H-2A_β : bm12) were highly or moderately effective in suppressing EAT outgrowth in B6-nu/nu, and in the latter combination of B6. C-H2^<bm12> and B6-nu/nu, the recipient showed GVHD. In contrast, activated spleen cells from B6 mice were ineffective in suppressing EAT outgrowth in ddY-prg (H-2^q) or in ICR-nu/nu (H-2^<q/?>) mice. In other combinations such as B10 (H-2^b) and B10.BR (H-2^k), adoptive immune transfer was unsuccessful. Adoptive immune transfer from B10.D2 (H-2^b) to DBA/2 (H-2^d) was also unsuccessful, though the donor and recipient share the same H-2 genes. Transfer from BALB/c (H-2^d) to DBA/2 (H-2^d) also failed even though they have similar genetic profile. On the other hand, activated spleen cells from B6 and from C3H were ineffective in suppressing EAT outgrowth in the hybrid; [B6×C3H] F_1. With this combination, the recipient showed GVHD. The results indicated the following : 1) Adoptive immunity to EAT was successfully transferred from B6 mice to B6-nu/nu mice, and some genetic shifts in TL or Ly haplotypes in the donor interferred slightly with the effectiveness. 2) Between the allogeneic inbred mouse strains, adoptive immune transfer was unsuccessful even between a donor and recipient combination which share the same H-2 haplotype, suggesting interference by other genes such as the minor histocompatibility gene. 3) GVHD occurred in some ineffective recipients but not in other ineffective ones, indicating the existence of two different interactions between donor spleen cells and recipient defense mechanisms which disturb the immune transfer.
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Evaluation of Adoptive Immunotherapy for Ehrlich Tumors in Mice

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