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*
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105;
Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and
Department of Pathology, University of Tennessee, Memphis, TN 38163
Like EBV-infected humans with infectious mononucleosis, mice
infected with the rodent gammaherpesvirus MHV-68 develop a profound
increase in the number of CD8+ T cells in the circulation.
In the mouse model, this lymphocytosis consists of highly activated
CD8+ T cells strikingly biased toward V
4 TCR expression.
Moreover, this expansion of V4+CD8+ T cells
does not depend on the MHC haplotype of the infected animal. Using a
panel of lacZ-inducible T cell hybridomas, we have
detected V4-specific T cell stimulatory activity in the spleens of
MHV-68-infected mice. We show that the appearance and quantity of this
activity correlate with the establishment and magnitude of latent viral
infection. Furthermore, on the basis of Ab blocking studies as well as
experiments with MHC class II, 2-microglobulin
(2m) and TAP1 knockout mice, the V4-specific T cell
stimulatory activity does not appear to depend on conventional
presentation by classical MHC class I or class II molecules. Taken
together, the data indicate that during latent infection, MHV-68 may
express a T cell ligand that differs fundamentally from both
conventional peptide Ags and classical viral
superantigens.
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