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David H. Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, University of Rochester, Rochester, NY 14642;
Istituto Superiore di Sanita, Rome, Italy;
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105; and
Division of Immunology, Walter and Eliza Hall Institute of Medical Research, PO Royal Melbourne Hospital, Melbourne, Victoria, Australia
The role of Ag in the recruitment and localization of naive,
acutely activated, and memory CD8+ T cells to the lung
during influenza infection was explored using TCR-transgenic (Tg) mice.
Naive, Thy1.2+CD8+ OT-I TCR-Tg cells
were primed and recruited to the lung after transfer into congenic
Thy1.1+ recipients challenged with a genetically engineered
influenza virus (influenza A/WSN/33 (WSN)-OVAI)
containing the Kb restricted OVA257–264
epitope (siinfekl) in the viral neuraminidase stalk. However, if the
transferred animals were infected with a similar influenza virus that
expressed an irrelevant Kb epitope (WSN-PEPII), no TCR-Tg T
cells were detectable in the lung, although they were easily visible in
the lymphoid organs. Conversely, there were substantial numbers of OT-I
cells found in the lungs of WSN-PEPII-infected mice when the animals
had been previously, or were concurrently, infected with a recombinant
vaccinia virus expressing OVA. Similar results were obtained with
nontransgenic populations of memory CD8+ T cells reactive
to a murine 
-herpesvirus-68 Ag. Interestingly, the primary host
response to the immunodominant influenza nucleoprotein epitope was not
affected by the presence of memory or recently activated OT-I T cells.
Thus, although Ag is required to activate the T cells, the subsequent
localization of T cells to the lung during a virus infection is a
property of recently activated and memory T cells and is not
necessarily driven by Ag in the lung.
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