| First Author | Matsuo M | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 11 | Pages | 6420-5 |
| PubMed ID | 10352255 | Mgi Jnum | J:55068 |
| Mgi Id | MGI:1337199 | Doi | 10.4049/jimmunol.162.11.6420 |
| Citation | Matsuo M, et al. (1999) Expression of multiple unique rejection antigens on murine leukemia BALB/c RLmale symbol1 and the role of dominant Akt antigen for tumor escape. J Immunol 162(11):6420-5 |
| abstractText | Using the pRL1a Ag-loss RL male 1 tumor variant cell line RM2-1, we demonstrated the presence of tumor Ags other than pRL1a that were recognized by CTLs on RL male 1 cells, Semiallogeneic CB6F(1) or syngeneic BALB/c CTLs generated against RM2-1 lysed RM2-1 and RL male 1 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 RL male 1 and limiting dilution analysis suggested that the pRL1a peptide was dominantly recognized to the RM2-1 peptides by CTLs on RL male 1 cells, The rejection response against the parental RL male 1 tumor was much less than that against RM2-1 cells in either CB6F(1) 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 RL male 1. Depletion of CD4 T cells caused the regression of RL male 1 at the doses in which the tumor grew in untreated-mice. The generation of pRL1a CTLs was inhibited in RL male 1-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 RL male 1. |
