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¹ Department of Human Genetics, ² McGill Centre for the Study of Host Resistance, ³ Department of Microbiology and Immunology, McGill University, Montreal, Quebec, H3A 1B1, Canada
⁴ Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143
⁵ School of Medicine, University of Rijeka, HR-51 000 Rijeka, Croatia
⁶ Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, OR 97239
⁷ Max von Pettenkofer-Institut, 80336 Munich, Germany

CORRESPONDENCE Silvia M. Vidal: silvia.vidal{at}mcgill.ca

Natural killer (NK) cells are crucial in resistance to certain viral infections, but the mechanisms used to recognize infected cells remain largely unknown. Here, we show that the activating Ly49P receptor recognizes cells infected with mouse cytomegalovirus (MCMV) by a process that requires the presence of H2-D^k and the MCMV m04 protein. Using H2 chimeras between H2-D^b and -D^k, we demonstrate that the H2-D^k peptide-binding platform is required for Ly49P recognition. We identified m04 as a viral component necessary for recognition using a panel of MCMV-deletion mutant viruses and complementation of m04-deletion mutant (m04) virus infection. MA/My mice, which express Ly49P and H2-D^k, are resistant to MCMV; however, infection with m04 MCMV abrogates resistance. Depletion of NK cells in MA/My mice abrogates their resistance to wild-type MCMV infection, but does not significantly affect viral titers in mice infected with m04 virus, implicating NK cells in host protection through m04-dependent recognition. These findings reveal a novel mechanism of major histocompatability complex class I–restricted recognition of virally infected cells by an activating NK cell receptor.

© 2009 Kielczewska et al.
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This article has been cited by other articles:

• Lemmermann, N. A. W., Gergely, K., Bohm, V., Deegen, P., Daubner, T., Reddehase, M. J. (2010). Immune Evasion Proteins of Murine Cytomegalovirus Preferentially Affect Cell Surface Display of Recently Generated Peptide Presentation Complexes. J. Virol. 84: 1221-1236 [Abstract] [Full Text]  

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