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Trudeau Institute, Saranac Lake, NY 12983
Previous studies have shown that vaccine-primed CD4+ T
cells can mediate accelerated clearance of respiratory virus infection.
However, the relative contributions of Ab and CD8+ T cells,
and the mechanism of viral clearance, are poorly understood. Here we
show that control of a Sendai virus infection by primed
CD4+ T cells is mediated through the production of IFN-
and does not depend on Ab. This effect is critically dependent on
CD8+ cells for the expansion of CD4+ T cells in
the lymph nodes and the recruitment of memory CD4+ T cells
to the lungs. Passive transfer of a CD8+ T cell supernatant
into CD8+ T cell-depleted, hemagglutinin-neuraminidase
(HN)421–436-immune µMT mice substantially restored the
virus-specific memory CD4+ response and enhanced viral
control in the lung. Together, the data demonstrate for the first time
that in vivo primed CD4+ T cells have the capacity to
control a respiratory virus infection in the lung by an Ab-independent
mechanism, provided that CD8+ T cell "help" in the form
of soluble factor(s) is available during the virus infection. These
studies highlight the importance of synergistic interactions between
CD4+ and CD8+ T cell subsets in the generation
of optimal antiviral immunity.
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