HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rodriguez, M. Articles by Brown, M. G. Search for Related Content PubMed PubMed Citation Articles by Rodriguez, M. Articles by Brown, M. G.

Cmv1-Independent Antiviral Role of NK Cells Revealed in Murine Cytomegalovirus-Infected New Zealand White Mice¹

Marisela Rodriguez^*, Pearl Sabastian, Patricia Clark and Michael G. Brown^2,*,

Departments of ^* Microbiology and Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA 22908

Ly49H⁺ NK cells play a critical role in innate antiviral immune responses to murine CMV (MCMV). Ly49H^b6 recognition of MCMV-encoded m157 on infected cells activates natural killing required for host resistance. We show that mAb 3D10 (anti-Ly49H) recognizes comparable subsets of NK cells from New Zealand White (NZW), New Zealand Black (NZB), and C57BL/6 spleens. However, virus levels in the spleens of MCMV-infected NZW and NZB mice differed greatly. We found that MCMV replication in infected NZW spleens was limited through NK cells. Alternately, NZB mice were profoundly susceptible to MCMV infection. Although 3D10 mAb injections given before infection interfere with Cmv1-type resistance in C57BL/6 mice, similar mAb injections did not affect NZW resistance, likely because NZW NK cell receptors did not bind MCMV-encoded m157. Instead, anti-MCMV host defenses in hybrid NZ offspring were associated with multiple chromosome locations including several putative quantitative trait loci that did not overlap with H-2 or NK gene complex loci. This study revealed a novel pathway used by NK cells to defend against MCMV infection. Thus, the importance of Ly49H in MCMV infection may be shaped by other additional background genes.

This article has been cited by other articles:

				X. Xie, M. D. Stadnisky, and M. G. Brown MHC Class I Dk Locus and Ly49G2+ NK Cells Confer H-2k Resistance to Murine Cytomegalovirus J. Immunol., June 1, 2009; 182(11): 7163 - 7171. [Abstract] [Full Text] [PDF]

				A. H. Davis, N. V. Guseva, B. L. Ball, and J. W. Heusel Characterization of Murine Cytomegalovirus m157 from Infected Cells and Identification of Critical Residues Mediating Recognition by the NK Cell Receptor Ly49H J. Immunol., July 1, 2008; 181(1): 265 - 275. [Abstract] [Full Text] [PDF]

				X. Xie, A. Dighe, P. Clark, P. Sabastian, S. Buss, and M. G. Brown Deficient Major Histocompatibility Complex-Linked Innate Murine Cytomegalovirus Immunity in MA/My.L-H2b Mice and Viral Downregulation of H-2k Class I Proteins J. Virol., January 1, 2007; 81(1): 229 - 236. [Abstract] [Full Text] [PDF]

				A. Dighe, M. Rodriguez, P. Sabastian, X. Xie, M. McVoy, and M. G. Brown Requisite H2k Role in NK Cell-Mediated Resistance in Acute Murine Cytomegalovirus-Infected MA/My Mice J. Immunol., November 15, 2005; 175(10): 6820 - 6828. [Abstract] [Full Text] [PDF]