Maternal transfer of infectious mouse mammary tumor retroviruses does not depend on clonal deletion of superantigen‐reactive Vβ14+T cells

摘要

AbstractFemale C3H/HeJ mice maternally transmit through their milk an infectious mouse mammary tumor retrovirus (MMTV) which causes clonal deletion of T cell receptor (TcR)Vβ14+T cells reactive to the retroviral superantigen (SAG). To test whether CD4+or CD8+T cells are crucial for intestinal infection and maternal transfer of exogenous retroviruses, newborn mice lacking CD4 or CD8 molecules after gene targetting were raised by surrogate C3H/HeJ mothers. In CD8−/−mice, clonal deletion of TcRVβ14+cells reactive to the SAG from this exogenous MMTV occured with delayed kinetics. Deletion of TcRVβ14+cells was not observed in CD4−/−mice up to 12 months after exposure to the retrovirus. In both CD4−/−and CD8−/−mice TcRVβ5+and TcRVβ11+T cells were deleted in the presence of genomically integrated endogenous MMTV (Mtv), indicating that the lack of SAG‐induced clonal deletion was not due to a general defect in these mutant mouse strains. Although TcRVβ14+T cells were not deleted in CD4−/−mice, female CD4−/−mice nursed on C3H/HeJ milk maternally transmitted the retrovirus to their offspring, albeit with delayed kinetics. These data demonstrate that CD4+and CD8+lymphocytes influence clonal deletion events and that the mechanisms responsible for clonal deletion of SAG‐reactive TcRVβ14+T cells may be different from mechanisms which allow the mammary tumor virus to enter the mammary gland