Imprint of human cytomegalovirus infection on the NK cell receptor repertoire.

@article{Guma2004ImprintOH,
  title={Imprint of human cytomegalovirus infection on the NK cell receptor repertoire.},
  author={M{\'o}nica Guma and Ana Angulo and Carlos Vilches and Natalia Gómez-Lozano and N{\'u}ria Malats and Miguel L{\'o}pez-Botet},
  journal={Blood},
  year={2004},
  volume={104 12},
  pages={
          3664-71
        },
  url={https://api.semanticscholar.org/CorpusID:6213977}
}
Data support that HCMV infection selectively shapes the natural killer cell receptor (NKR) repertoire of NK and T cells from healthy carrier individuals.
View on PubMed
ashpublications.org
820 Citations
Highly Influential Citations
43
Background Citations
282
Methods Citations
12
Results Citations
28

Figures and Tables from this paper

820 Citations

Influence of human cytomegalovirus infection on the NK cell receptor repertoire in children

Data reveal that hCMV may have a profound influence on the NKR repertoire in early childhood, and excretion of the virus was associated with higher proportions of NKG2C+ NK cells.

NK cell receptors involved in the response to human cytomegalovirus infection.

Human cytomegalovirus infection is a paradigm of the complexity reached by host-pathogen interactions, and HCMV interferes with the expression of NKG2D ligands in infected cells to escape from NK cell-mediated surveillance.

Expression and function of NKG2D in CD4+ T cells specific for human cytomegalovirus

The data support the notion that NKG2D functions as a prototypic costimulatory receptor in a subset of HCMV‐specific CD4+ T lymphocytes and thus may have a role in the response against infected HLA class II+ cells displaying NKG 2D ligands.

Human cytomegalovirus infection is associated with increased proportions of NK cells that express the CD94/NKG2C receptor in aviremic HIV-1-positive patients.

The conclusion that changes in the NKR repertoire in HIV1-positive patients are related to a concomitant HCMV infection is supported.

Expansion of CD94/NKG2C+ NK cells in response to human cytomegalovirus-infected fibroblasts.

The data support that the interaction of CD94/NKG2C with HCMV-infected fibroblasts, concomitant to the inhibition of human leukocyte antigen (HLA) class I expression, promotes an outgrowth of CD 94/NKg2C(+) NK cells.

Influence of congenital human cytomegalovirus infection and the NKG2C genotype on NK‐cell subset distribution in children

Novel insights are provided on the impact of HCMV infection on the homeostasis of the NK‐cell compartment in children, revealing a modulatory influence of NKG2C copy number.

NK cell responses to cytomegalovirus infection lead to stable imprints in the human KIR repertoire and involve activating KIRs.

The results provide new insight into the diversity of KIR repertoire and its adaptation to virus infection, suggesting a role for both activating and inhibitory KIRs in immunity to CMV infection.

The CD94/NKG2C+ NK-cell subset on the edge of innate and adaptive immunity to human cytomegalovirus infection.

ArticleCytomegalovirus-driven Adaption of Natural Killer Cells in NKG

The general phenotypic and functional equivalency observed suggests NKG2C-independent routes of HCMV-driven NK cell differentiation, which may involve increased CD2 expression, are suggested.

Activating KIRs and NKG2C in Viral Infections: Toward NK Cell Memory?

The persistent, HCMV-induced, imprinting suggests that NK cells may display unexpected adaptive immune traits, and the role of aKIRs and NKG2C in regulating NK cell responses and promoting a memory-like response to certain viruses is discussed.
...

62 References

Natural killer cell receptors for major histocompatibility complex class I and related molecules in cytomegalovirus infection.

Three aspects of the host-pathogen interaction are reviewed, including downmodulation of major histocompatibility complex class I molecules by cytomegalovirus, NK-activating receptors specific to ligands expressed on virus-infected cells, and the expression of ligands for NKG2D are reviewed.

HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C

The identification of ligands for HLA-E is reported, which shows that a subset of HLA class I alleles has been shown to inhibit killing by CD94/NKG2A+ NK-cell clones, and only the HLA alleles that possess a leader peptide capable of upregulating Hla-E surface expression confer resistance toNK-cell-mediated lysis.

HLA-E is a major ligand for the natural killer inhibitory receptor CD94/NKG2A.

Examination of HLA-E antigen distribution indicated that it is detectable on the surface of a wide variety of cell types, consistent with the prediction that the ligand for CD94/NKG2A is expressed ubiquitously.

Differentiation of cytomegalovirus-specific CD8(+) T cells in healthy and immunosuppressed virus carriers.

Data show that in response to immunosuppressive medication quantitative and qualitative changes occur in the CD8(+) T-cell compartment, and these adaptations may be instrumental to maintain CMV latency.

Variations of human killer cell lectin-like receptors: common occurrence of NKG2-C deletion in the general population

Although human NKG2-A, -C and CD94 are generally conserved with respect to amino acid sequences, NKG 2-A is polymorphic in the noncoding region, and that the number of genes encoded in the human NKC is variable among individuals, as previously shown for the leukocyte receptor complex (LRC), HLA and Fcγ receptor (FCGR) regions.

Functionally and structurally distinct NK cell receptor repertoires in the peripheral blood of two human donors.

Costimulation of CD8alphabeta T cells by NKG2D via engagement by MIC induced on virus-infected cells.

It is found that infection by cytomegalovirus resulted in substantial increases in MIC on cultured fibroblast and endothelial cells and was associated with induced MIC expression in interstitial pneumonia and NKG2D functioned as a costimulatory receptor that can substitute for CD28.

Human Cytomegalovirus Glycoprotein UL16 Causes Intracellular Sequestration of NKG2D Ligands, Protecting Against Natural Killer Cell Cytotoxicity

The intracellular sequestration of NKG2D ligands by UL16 represents a novel HCMV immune evasion mechanism to add to the well-documented viral strategies directed against antigen presentation by classical MHC molecules.

Surface expression of HLA-E, an inhibitor of natural killer cells, enhanced by human cytomegalovirus gpUL40.

It is shown that, independently of the transporter associated with antigen processing, gpUL40 can up-regulate expression of HLA-E, which protects _targets from NK cell lysis, which is up-regulated by HCMV.

Effects of Human Cytomegalovirus Infection on Ligands for the Activating NKG2D Receptor of NK Cells: Up-Regulation of UL16-Binding Protein (ULBP)1 and ULBP2 Is Counteracted by the Viral UL16 Protein1

It is shown that upon infection with HCMV, the host cell responds by expression of ULBPs and increased susceptibility to the NKG2D-mediated component of NK cell recognition, but UL16 limits these effects by interfering with the surface expression of ULBP1 and ULBP2.
...

Related Papers

Showing 1 through 3 of 0 Related Papers