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From the * Laboratoire d'Immunologie, Institut de Recherches Cliniques de Montréal, H2W 1R7
Montréal, Canada; Transfer of vSAG7, the endogenous superantigen encoded in the Mtv7 locus, from MHC class
II Laboratoire d'Immunochimie Analytique, Institut Pasteur, 75015 Paris, France;
and § Department of Microbiology and Immunology, Universite de Montréal, H3C 3J7 Montréal,
Canada and Department of Microbiology and Immunology, and Department of Experimental
Medicine, McGill University, H3A 2B4 Montréal, Canada
to MHC class II+ cells has been suggested to occur both in vivo and in vitro. This transfer
usually leads to the activation and deletion of T cells expressing responsive V
s. However,
there is no direct molecular evidence for such a transfer. We have developed an in vitro system
which confirms this property of vSAGs. vSAG7 was transfected into a class II murine fibroblastic line. Coculture of these cells with class II+ cells and murine T cell hybridomas expressing the specific Vs led to high levels of IL-2 production which was specifically inhibited by
vSAG7- and MHC class II-specific mAbs. Moreover, injection of vSAG7+ class II cells in
mice led to expansion of V6+ CD4+ cells. We show that this transfer activity is paracrine but
does not require cell-to-cell contact. Indeed, vSAG7 was transferred across semi-permeable
membranes. Transfer can occur both from class II and class II+ cells, indicating that MHC
class II does not sequester vSAG7. Finally, competition experiments using bacterial toxins with
well defined binding sites showed that the transferred vSAG7 fragment binds to the 
1 domain
of HLA-DR.
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