RGD Reference Report - Activating NK cell receptor expression/function (NKp30, NKp46, DNAM-1) during chronic viraemic HCV infection is associated with the outcome of combined treatment. - Rat Genome Database

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Activating NK cell receptor expression/function (NKp30, NKp46, DNAM-1) during chronic viraemic HCV infection is associated with the outcome of combined treatment.

Authors: Bozzano, Federica  Picciotto, Antonino  Costa, Paola  Marras, Francesco  Fazio, Valentina  Hirsch, Ivan  Olive, Daniel  Moretta, Lorenzo  De Maria, Andrea 
Citation: Bozzano F, etal., Eur J Immunol. 2011 Oct;41(10):2905-14. doi: 10.1002/eji.201041361.
RGD ID: 40818295
Pubmed: PMID:21695691   (View Abstract at PubMed)
DOI: DOI:10.1002/eji.201041361   (Journal Full-text)

Specific NK cell killer inhibitory receptor (KIR):HLA haplotype combinations have been associated with successful clearance of acute and chronic HCV infection. Whether an imbalance of activating NK cell receptors also contributes to the outcome of treatment of chronic HCV infection, however, is not known. We studied peripheral NK cell phenotype and function in 28 chronically viraemic HCV genotype I treatment-naïve patients who underwent treatment with pegylated IFN-α and ribavirin. At baseline, chronically infected patients with sustained virological response (SVR) had reduced CD56(bright) CD16(+/-) cell populations, increased CD56(dull) CD16(+) NK cell proportions, and lower expression of NKp30, DNAM-1, and CD85j. Similarly, reduced NK cell IFN-γ production but increased degranulation was observed among nonresponding (NR) patients. After treatment, CD56(bright) CD16(+/-) NK cell numbers increased in both SVR and NR patients, with a parallel significant increase in activating NKp30 molecule densities in SVR patients only. In vitro experiments using purified NK cells in the presence of rIL-2 and IFN-α confirmed upregulation of NKp30 and also of NKp46 and DNAM-1 in patients with subsequent SVR. Thus, differences in patient NK cell receptor expression and modulation during chronic HCV-1 infection are associated with subsequent outcome of standard treatment. Individual activating receptor expression/function integrates with KIR:HLA genotype carriage to determine the clearance of HCV infection upon treatment.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CD226HumanChronic Hepatitis C treatmentIEP  RGD 
Cd226MouseChronic Hepatitis C treatmentISOCD226 (Homo sapiens) RGD 
NCR1HumanChronic Hepatitis C treatmentIEP  RGD 
NCR3HumanChronic Hepatitis C treatmentIEP  RGD 
Ncr1RatChronic Hepatitis C treatmentISONCR1 (Homo sapiens) RGD 
Ncr1MouseChronic Hepatitis C treatmentISONCR1 (Homo sapiens) RGD 
Ncr3RatChronic Hepatitis C treatmentISONCR3 (Homo sapiens) RGD 
Ncr3-psMouseChronic Hepatitis C treatmentISONCR3 (Homo sapiens) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ncr1  (natural cytotoxicity triggering receptor 1)
Ncr3  (natural cytotoxicity triggering receptor 3)

Genes (Mus musculus)
Cd226  (CD226 antigen)
Ncr1  (natural cytotoxicity triggering receptor 1)
Ncr3-ps  (natural cytotoxicity triggering receptor 3, pseudogene)

Genes (Homo sapiens)
CD226  (CD226 molecule)
NCR1  (natural cytotoxicity triggering receptor 1)
NCR3  (natural cytotoxicity triggering receptor 3)


Additional Information