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*
Laboratory of Host Defense, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan;
First Department of Surgery, Gunma University School of Medicine, Maebashi, Japan;
Sections of Infectious Diseases and Immunology, Yale University School of Medicine, New Haven, CT 06520;
Infectious Disease Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, Immunology Program, Sloan-Kettering Institue, New York, NY 10021
To elucidate potential roles of IL-15 in the maintenance of memory
CD8+ T cells, we followed the fate of Ag-specific
CD8+ T cells directly visualized with MHC class I tetramers
coupled with listeriolysin O (LLO)91–99 in IL-15
transgenic (Tg) mice after Listeria monocytogenes
infection. The numbers of LLO91–99-positive memory
CD8+ T cells were significantly higher at 3 and 6 wk after
infection than those in non-Tg mice. The LLO91–99-positive
CD8+ T cells produced IFN-
in response to
LLO91–99, and an adoptive transfer of CD8+ T
cells from IL-15 Tg mice infected with L. monocytogenes
conferred a higher level of resistance against L.
monocytogenes in normal mice. The
CD44+CD8+ T cells from infected IL-15 Tg mice
expressed the higher level of Bcl-2. Transferred
CD44+CD8+ T cells divided more vigorously in
naive IL-15 Tg mice than in non-Tg mice. These results suggest that
IL-15 plays an important role in long-term maintenance of Ag-specific
memory CD8+ T cells following microbial exposure via
promotion of cell survival and homeostatic
proliferation.
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