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Journal of Virology, November 2001, p. 10746-10754, Vol. 75, No. 22
Department of Microbiology and Immunology and
The Walther Oncology Center, The Walther Cancer Institute, Indiana
University School of Medicine, Indianapolis, Indiana
46202,1 and Department of Cell
Biology, Neurobiology, and Anatomy, University of Cincinnati College
of Medicine, Cincinnati, Ohio 452672
Received 20 April 2001/Accepted 11 August 2001
Natural killer T (NKT) cells, a unique subpopulation of T cells,
coexpress markers also present on NK cells and recognize the major
histocompatibility complex class I-like CD1d1 molecule. We studied the
effect of an acute virus infection on NKT cells. Mice were infected
with the nonhepatotropic Armstrong strain of lymphocytic
choriomeningitis virus (LCMV), and at various times postinfection,
mononuclear cells from the liver, peritoneum, and spleen were isolated.
It was found that within 2 to 3 days, there was a selective loss of NKT
cells from the liver with an apparent rapid recovery within 8 to 14 days. There was no increase in peritoneal or splenic NKT cells,
indicating that NKT cells did not traffic to these tissues. This loss
of NKT cells was independent of gamma interferon (IFN-
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.22.10746-10754.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Selective Loss of Natural Killer T Cells by
Apoptosis following Infection with Lymphocytic Choriomeningitis
Virus
) and
interleukin 12 (IL-12) production, but did occur in mice treated with
poly(I-C), a classical inducer of IFN-
/
. The reduction in NKT
cells was CD28 and fas/fasL independent and occurred via apoptosis. It was not observed in LCMV-infected DNA
fragmentation factor 45-deficient mice, and an increase in active
caspase 3-specific staining was found in liver NKT cells from
LCMV-infected and poly(I-C)-treated mice compared to uninfected wild-type mice. Interestingly, it was also found that liver NKT cells
from LCMV-infected mice were themselves infected. These results suggest
that the loss of NKT cells following an acute LCMV infection could be
due to the induction of IFN-
/
resulting in NKT-cell apoptosis and
is important for the host's immune response to LCMV.
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Indiana University School of Medicine,
Building R4, Rm. 302, 1044 W. Walnut St., Indianapolis, IN 46202-5254. Phone: (317) 274-7589. Fax: (317) 274-7592. E-mail:
rbrutkie{at}iupui.edu.
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