Generation of anti-AKR/gross murine leukemia virus cytotoxic T lymphocytes (CTL) . An analysis of precursor CTL frequencies in the AKR.H-2b and C57BL/6 mouse strains
Wegmann, K.W.; Rich, R.F.; Green, W.R.
Journal of Immunology 149(5): 1593-1598
1992
ISSN/ISBN: 0022-1767 PMID: 1324278 Document Number: 399274
C57BL/6 mice, after immunization and secondary in vitro restimulation with AKR/Gross murine leukemia virus (MuLV)-induced tumors, generate AKR/Gross MuLV-specific CTL. After similar immunization protocols, AKR-H-2-b mice fail to generate CTL specific for AKR/Gross MuLV. The basis for nonresponsiveness in AKR.H-2-b mice is unknown, however, unlike C57BL/6 mice, AKR.H-2-b mice carry endogenous proviruses and express N-ecotropic viral Ag. Thus, clonal deletion of pCTL populations due to the expression of AKR/Gross MuLV-like Ag is a likely mechanism for the nonresponsiveness. To determine if nonresponsiveness is due to clonal deletion, limiting dilution cultures were performed to assess the presence of pCTL specific for AKR/Gross MuLV. Our study demonstrates that the frequencies of pCTL specific for AKR/Gross MuLV are similar in both the responder C57BL/6 and nonresponder AKR.H-2-b strains. The observation that normal levels of AKR/Gross MuLV-specific pCTL exist in AKR.H-2-b mice, suggests that clonal deletion of pCTL is not responsible for the inability of AKR.H-2-b mice to generate anti-AKR/Gross virus-specific CTL.