English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The cytomegalovirus resistance locus  Cmv3  has been linked to an epistatic interaction between two loci: a Natural Killer (NK) cell receptor gene and the major histocompatibility complex class I (MHC-I) locus. To demonstrate the interaction between  Cmv3  and  H2 k  , we generated double congenic mice between MA/My and BALB.K mice and an F 2  cross between FVB/N ( H-2 q  ) and BALB.K ( H2 k  ) mice, two strains susceptible to mouse cytomegalovirus (MCMV). Only mice expressing  H2 k   in conjunction with  Cmv3 MA/My   or  Cmv3 FVB   were resistant to MCMV infection. Subsequently, an F 3  cross was carried out between transgenic FVB/ H2-D k   and MHC-I deficient mice in which only the progeny expressing  Cmv3 FVB   and a single  H2-D k   class-I molecule completely controlled MCMV viral loads. This phenotype was shown to be NK cell–dependent and associated with subsequent NK cell proliferation. Finally, we demonstrated that a number of  H2 q   alleles influence the expression level of  H2 q   molecules, but not intrinsic functional properties of NK cells; viral loads, however, were quantitatively proportional to the number of  H2 q   alleles. Our results support a model in which  H-2 q   molecules convey Ly49-dependent inhibitory signals that interfere with the action of  H2 -D k  on NK cell activation against MCMV infection. Thus, the integration of activating and inhibitory signals emanating from various MHC-I/NK cell receptor interactions regulates NK cell–mediated control of viral load.

NK Cell Receptor/H2-Dk–Dependent Host Resistance to Viral Infection Is Quantitatively Modulated by H2q Inhibitory Signals