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Journal of Experimental Medicine, Vol 174, 875-880, Copyright © 1991 by Rockefeller University Press
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M Eichelberger, W Allan, M Zijlstra, R Jaenisch and PC Doherty
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.
Transgenic mice homozygous for a beta 2-microglobulin (beta 2-m) gene disruption and normal mice that had been treated with a CD8-specific mAb were infected intranasally with an H3N2 influenza A virus. Both groups of CD8T cell-deficient mice eliminated the virus from the infected respiratory tract. Potent CTL activity was detected in lung lavage populations taken from mice with intact CD8+ T cell function, with minimal levels of cytotoxicity being found for inflammatory cells obtained from the antibody-treated and beta 2-m mutant mice. We therefore conclude that cells infected with an influenza A virus can be cleared from the respiratory tract of mice lacking both functional class I major histocompatibility complex (MHC) glycoproteins and class I MHC-restricted, CD8+ effector T cells.
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