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© The Rockefeller University Press, 0022-1007/1997/6/1969/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 11, June 2, 1997 1969-1975


Article

T Cell Receptor–{gamma}/{delta} Cells Protect Mice from Herpes Simplex Virus Type 1–induced Lethal Encephalitis

Roger Sciammas*, P. Kodukula{ddagger}, Q. Tang{ddagger}, R.L. Hendricks{ddagger}, and J.A. Bluestone*

From the * Ben May Institute for Cancer Research, Department of Pathology and Committee on Immunology, University of Chicago, Chicago, Illinois 60637; and the {ddagger} Department of Ophthalmology Visual Sciences and Department of Pathology, University of Illinois at Chicago, Chicago, Illinois 60612

Increased numbers of T cell receptor (TCR)-{gamma}/{delta} cells have been observed in animal models of influenza and sendai virus infections, as well as in patients infected with human immunodeficiency virus and herpes simplex virus type 1 (HSV-1). However, a direct role for TCR-{gamma}/{delta} cells in protective immunity for pathogenic viral infection has not been demonstrated. To define the role of TCR-{gamma}/{delta} cells in anti–HSV-1 immunity, TCR-{alpha}–/– mice treated with anti– TCR-{gamma}/{delta} monoclonal antibodies or TCR-{gamma}/{delta} x TCR-{alpha}/β double-deficient mice were infected with HSV-1 by footpad or ocular routes of infection. In both models of HSV-1 infection, TCR-{gamma}/{delta} cells limited severe HSV-1–induced epithelial lesions and greatly reduced mortality by preventing the development of lethal viral encephalitis. The observed protection resulted from TCR-{gamma}/{delta} cell–mediated arrest of both viral replication and neurovirulence. The demonstration that TCR-{gamma}/{delta} cells play an important protective role in murine HSV-1 infections supports their potential contribution to the immune responses in human HSV-1 infection. Thus, this study demonstrates that TCR-{gamma}/{delta} cells may play an important regulatory role in human HSV-1 infections.


Address correspondence to Jeffrey A. Bluestone, Ben May Institute for Cancer Research, University of Chicago, MC 1089, 5841 S. Maryland Ave., Chicago, IL 60637.

R. Sciammas is supported by a National Institutes of Health/National Institute of Allergy and Infectious Diseases interdisciplinary training program in immunology No. 5T32A107090, J. Bluestone is supported by a grant from the National Institutes of Health No. RO1 AI26847, and P. Kodukula, Q. Tang, and R.L. Hendricks are supported by grants from the National Institutes of Health No. EY10359, EY05945, and EY01792.

R. Sciammas and P. Kodukula contributed equally to this work.

1Abbreviations used in this paper: HSK, herpetic stromal keratitis; rh, recombinant human.


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