Changes of the immunogenic properties of K36 lymphoma treated in vivo with 5(3,3-dimethyl-1-triazeno) imidazole-4-carboxamide (DTIC)

Mice of AKR strain bearing syngeneic K36 lymphoma were treated with DTIC for a number of transplant generations. The lymphoma line (K36/DTIC) became resistant to DTIC treatment and weakly immunogenic for AKR or (AKR × DBA/2)F₁ hosts. Previous findings, however, showed that DTIC-treated H-2^b or H-2^b lymphomas became DTIC-resistant as well, but acquired strong immunogenicity for histocompatible hosts. Transplantation resistance of allogeneic mice against K36 or K36/DTIC lines injected i.p. or i.v. was also investigated. Both lines inoculated i.p. were rejected by either H-2-incompatible recipients, or H-2-compatible mice incompatible for minor histocompatibility loci (MIH). When the tumors were injected intravenously, H-2-compatible MIH-incompatible mice were more susceptible than H-2-MIH-incompatible recipients to lymphoma challenge. Moreover K36/DTIC line elicited stronger transplantation resistance than K36 tumor. Unexpectedly H-2-MIH-incompatible mice homozygous for the H-2^d haplotype were partially susceptible to the i.v. challenge with K36 lymphoma cells. However, strong transplantation resistance was found in the same hosts against K36/DTIC line. In conclusion the limited increase of tumor cell immunogenicity obtained by treatment of K36 lymphoma with DTIC was detectable in syngeneic, hybrid and allogeneic mice.