Major and Minor Kb-Restricted Epitopes Encoded by the Endogenous Ecotropic Murine Leukemia Virus AKR623 That Are Recognized by Anti-AKR/Gross MuLV CTL

C57BL/6 mice can generate a type-specific and class I H-2K b -restricted CTL response against histocompatible AKR/Gross murine leukemia virus (MuLV) cell surface antigen positive (GCSA + ) tumor cells. These anti-AKR/Gross MuLV CTL are also known to lyse SC.K b /623 target cells expressing the molecular MuLV clone AKR623 (derived from the endogenous ecotropic MuLV provirus emv -11). To help identify AKR623 viral epitopes recognized by these CTL, four chimeric proviruses were constructed from two parental plasmids, pAKR623 and pAK7. It has been shown that SC.K b /7 fibroblast targets expressing the emv -14-derived molecular clone AK7 are only poorly lysed by anti-AKR/Gross MuLV CTL. Data from experiments employing SC.K b cells infected with the chimeras as targets against anti-AKR/Gross MuLV CTL supported the location of a previously identified immunodominant epitope located within the viral p15E transmembrane envelope protein, peptide TM134-141 (KSP-WFTTL). Furthermore, the use of K b -motif-defined AKR623 encoded peptides together with data obtained using the chimeric viruses allowed the identification of three additional anti-AKR/Gross MuLV CTL epitopes. Peptides representing these epitopes, MA125-132 (RSALYPAL), RT142-149 (SHRWYTVL), and RT456-463 (RMTHYQAM), are characterized herein with respect to their ability to confer lysis upon EMV− target cells and to stimulate tumor primed splenocytes in vitro . The identification and characterization of these additional epitopes allow for a better understanding of both the CTL response against GCSA + tumor cells and the dysfunctional CTL response against EMV-14 and AK7.