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*
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105; and
Department of Pathology, University of Tennessee, Memphis, TN 38163
A CD8+ T cell lymphocytosis in the peripheral blood is
associated with the establishment of latency following intranasal
infection with murine gammaherpesvirus-68. Remarkably, a large
percentage of the activated CD8+ T cells of mice expressing
different MHC haplotypes express Vß4+ TCR. Identification
of the ligand driving the Vß4+CD8+ T cell
activation remains elusive, but there is a general correlation between
Vß4+CD8+ T cell stimulatory activity and
establishment of latency in the spleen. In the current study, the role
of CD4+ T cells in the Vß4+CD8+ T
cell expansion has been addressed. The results show that
CD4+ T cells are essential for expansion of the
Vß4+CD8+ subset, but not other Vß subsets,
in the peripheral blood. CD4+ T cells are required
relatively late in the antiviral response, between 7 and 11 days after
infection, and mediate their effect independently of IFN-
.
Assessment of Vß4+CD8+ T cell stimulatory
activity using murine gammaherpesvirus-68-specific T cell hybridomas
generated from latently infected mice supports the idea that
CD4+ T cells control levels of the stimulatory ligand that
drives the Vß4+CD8+ T cells. As
Vß4+CD8+ T cell expansion also correlates
with levels of activated B cells, these data raise the possibility that
CD4+ T cell-mediated B cell activation is required for
optimal expression of the stimulatory ligand. In addition, in cases of
low ligand expression, there may also be a direct role for
CD4+ T cell-mediated help for
Vß4+CD8+ T cells.
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