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Cell. 1993 Aug 13;74(3):529-40.

Superantigen-induced immune stimulation amplifies mouse mammary tumor virus infection and allows virus transmission.

Author information

1
Ludwig Institute for Cancer Research, Lausanne Branch, Epalinges, Switzerland.

Abstract

Endogenous and infectious mouse mammary tumor viruses (MMTVs) encode in their 3' long terminal repeat a protein that exerts superantigen activity; that is, it is able to interact with T cells via the variable domain of the T cell receptor (TCR) beta chain. We show here that transmission of an infectious MMTV is prevented when superantigen-reactive cells are absent through either clonal deletion due to the expression of an endogenous MTV with identical superantigen specificity or exclusion due to expression of a transgenic TCR beta chain that does not interact with the viral superantigen. A strict requirement for superantigen-reactive T cells is also seen for a local immune response following MMTV infection. This immune response locally amplifies the number of MMTV-infected B cells, most likely owing to their clonal expansion. Collectively, our data indicate that a superantigen-induced immune response is critical for the MMTV life cycle.

PMID:
8394220
DOI:
10.1016/0092-8674(93)80054-i
[Indexed for MEDLINE]

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