Abstract
Mouse mammary tumor virus (MMTV), a replication-competent B-type murine retrovirus, causes mammary adenocarcinomas in some strains of laboratory mice and it can be transmitted exogenously via milk or endogenously through the germ line. It has been established that the immune system is directly involved in the infection pathway of MMTV, because thymectomy in neonates can decrease or delay mammary tumor incidence, and both T and B cells become infected with the virus. It has been shown that exogenous and endogenous MMTV have an open reading frame (ORF) encoding superantigen in the 3' long terminal repeat, which binds to MHC class II molecules and leads to stimulation and subsequent deletion of T cells bearing particular Vβ gene products.
MMTVORF product is a type II transmembrane molecules where the COOH-terminal is extracellular and the COOH-terminal is responsible for the Vβ specificity of the superantigens. As T cell recognition of superantigens is predominantly mediated by the TCR Vβ domain, superantigen can stimulate much higher proportions of T cells than conventional peptide antigens. This characteristic of superantigens plays an important role in infection with exogenous MMTV.
