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Department of Pathology, University of Massachusetts Medical Center, Worcester, MA 01655;
Department of Pathology, University of Texas, Southwestern, Dallas, TX; and
Frederick Cancer Research and Development Center, National Cancer Institute, Frederick, MD
The distributions and functions of NK cell subsets, as
defined by the expression of Ly49 NK cell receptors, were examined in
murine CMV (MCMV)-infected mice. MCMV induced a reduction in
NK1.1+ cell number in the spleen and an increase in the
peritoneal exudate cells. Within the splenic NK1.1+
population, proportional increases in Ly49A+ and
Ly49G2+ cells but decreases in Ly49C+ and
Ly49D+ cells were observed 3 days post-MCMV infection, but
within the peritoneal NK1.1+ cell populations there were
proportional decreases in Ly49A+ cells and increases in
Ly49C+, Ly49D+, and Ly49G2+ cells.
Lymphocytic choriomeningitis virus did not elicit a comparable NK cell
subset distribution. Lymphokine-activated killer cells were sorted into
different Ly49 NK cell subsets and adoptively transferred into C57BL/6
suckling mice. Regulation of MCMV synthesis in these suckling mice was
shown to be an IFN-
-dependent, perforin- and
Cmv-1-independent process, and each NK cell subset
mediated anti-viral activity. In adult C57BL/6 mice, the control of
MCMV in the spleen is mediated by a perforin-dependent mechanism,
regulated in part by the Cmv-1 gene, which maps closely
to the Ly49 family. In vivo depletions of either one or two of the Ly49
subsets in adult mice did not affect the ability of the residual NK
cells to regulate MCMV synthesis. These data provide evidence of NK
cell subset distribution and function in MCMV infection, but no
individual subset was required for the Cmv-1-like
regulation of MCMV synthesis.
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