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.
journal_name
Celljournal_title
Cellauthors
Held W,Waanders GA,Shakhov AN,Scarpellino L,Acha-Orbea H,MacDonald HRdoi
10.1016/0092-8674(93)80054-isubject
Has Abstractpub_date
1993-08-13 00:00:00pages
529-40issue
3eissn
0092-8674issn
1097-4172pii
0092-8674(93)80054-Ijournal_volume
74pub_type
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