Non-H-2 histocompatibility antigens encoded by Moloney-murine leukemia virus in Mov mouse strains are detectable by skin grafting and cytolytic T lymphocytes.

The integration and expression of Moloney-murine leukemia virus (M-MuLV) into the germ line of Mov mouse strains on the C57BL/6 background results in the expression of a cell-surface Ag with characteristics expected from non-H-2 histocompatibility Ag: the ability to stimulate graft rejection and generation of CTL. However, both the previously studied Mov-3 and Mov-14 strains differ from the coisogenic C57BL/6 strain by different length segments of chromosome derived from the ICR strain in addition to the integrated M-MuLV genome. To conclusively demonstrate that an Ag encoded by M-MuLV is solely responsible for rejection of Mov skin grafts by coisogenic recipients, we have studied additional Mov strains that differ from coisogenic 129 or BALB/c backgrounds only by integration of an M-MuLV genome. A total of 129 strain recipients reject skin grafts from two viremic Mov strains, Mov-17 and Mov-18. A total of 129 strain hosts primed with either 1) multiple sets of Mov-17 and Mov-18 skin grafts or 2) single injections of Mov-17 and Mov-18 spleen cells produce M-MuLV-specific CTL that could be boosted in primary mixed lymphocyte culture. Generated CTL were reactive with Con A-stimulated lymphoblasts from all tested viremic Mov strains on the B6 and 129 backgrounds as well as B6 lymphomas. Further, we have observed that 129 strain mice reject Mov-9 skin grafts if these skin grafts are transplanted to virgin 129 recipients which have not received prior skin grafts from non-viremic Mov donors. In addition, skin grafts were transplanted from two viremic Mov strains, Mov-15 and Mov-16, to coisogenic BALB/c recipients; rejection of both sets of grafts was observed. However, BALB/c responders did not generate specific CTL after priming in vivo, with either multiple sets of allogeneic grafts or spleen cell injections, and boosting in vitro. These observations confirm the ability of integrated and expressed M-MuLV genomes to encode what is operationally defined as a non-H-2 histocompatibility Ag.