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Expression of Multiple Unique Rejection Antigens on Murine Leukemia BALB/c RL1 and the Role of Dominant Akt Antigen for Tumor Escape¹

Mitsutoshi Matsuo^*,, Hisashi Wada^*, Shinichiro Honda^*, Isao Tawara^*, Akiko Uenaka^*, Takashi Kanematsu and Eiichi Nakayama^2,*

^* Department of Parasitology and Immunology, Okayama University Medical School, Okayama, Japan; and Department of Surgery II, Nagasaki University School of Medicine, Nagasaki, Japan

Using the pRL1a Ag-loss RL1 tumor variant cell line RM2-1, we demonstrated the presence of tumor Ags other than pRL1a that were recognized by CTLs on RL1 cells. Semiallogeneic CB6F₁ or syngeneic BALB/c CTLs generated against RM2-1 lysed RM2-1 and RL1 cells to a similar extent, but no killing was observed with any other tumor or normal cells examined. Clonal analysis and sensitization with reversed phase-HPLC fractions revealed that there were D^d- and L^d-binding peptides recognized by RM2-1 CTLs. Lysis by bulk CTLs stimulated against RL1 and limiting dilution analysis suggested that the pRL1a peptide was dominantly recognized to the RM2-1 peptides by CTLs on RL1 cells. The rejection response against the parental RL1 tumor was much less than that against RM2-1 cells in either CB6F₁ or BALB/c mice, suggesting that the presence of altered Akt molecules from which the dominant pRL1a peptide was derived inhibited the rejection response against RL1. Depletion of CD4 T cells caused the regression of RL1 at the doses in which the tumor grew in untreated mice. The generation of pRL1a CTLs was inhibited in RL1-bearing mice. Thus, immunoregulatory CD4 T cells were most likely activated by the altered Akt molecules and inhibited the efficient generation of CTLs against the dominant pRL1a Ag in RL1.