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Journal of Virology, November 2001, p. 10746-10754, Vol. 75, No. 22
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

Jacqueline A. Hobbs,1 Sungyoo Cho,1 Tonya J. Roberts,1 Venkataraman Sriram,1 Jianhua Zhang,2 Ming Xu,2 and Randy R. Brutkiewicz1,*

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-gamma ) and interleukin 12 (IL-12) production, but did occur in mice treated with poly(I-C), a classical inducer of IFN-alpha /beta . 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-alpha /beta 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.

Journal of Virology, November 2001, p. 10746-10754, Vol. 75, No. 22
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.22.10746-10754.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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