RGD Reference Report - Association of NKG2A with treatment for chronic hepatitis C virus infection. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Association of NKG2A with treatment for chronic hepatitis C virus infection.

Authors: Harrison, R J  Ettorre, A  Little, A-M  Khakoo, S I 
Citation: Harrison RJ, etal., Clin Exp Immunol. 2010 Aug;161(2):306-14. doi: 10.1111/j.1365-2249.2010.04169.x. Epub 2010 Jun 9.
RGD ID: 40818079
Pubmed: PMID:20550548   (View Abstract at PubMed)
PMCID: PMC2909413   (View Article at PubMed Central)
DOI: DOI:10.1111/j.1365-2249.2010.04169.x   (Journal Full-text)

Natural killer (NK) cells are critical to the immune response to viral infections. Their functions are controlled by receptors for major histocompatibility complex (MHC) class I, including NKG2A and killer-cell immunoglobulin-like receptors (KIR). In order to evaluate the role of MHC class I receptors in the immune response to hepatitis C virus infection we have studied patients with chronic HCV infection by multi-parameter flow cytometry directly ex vivo. This has permitted evaluation of combinatorial expression of activating and inhibitory receptors on single NK cells. Individuals with chronic HCV infection had fewer CD56(dim) NK cells than healthy controls (4.9 +/- 3.4% versus 9.0 +/- 5.9%, P < 0.05). Expression levels of the inhibitory receptor NKG2A was up-regulated on NK cells from individuals with chronic hepatitis C virus (HCV) (NKG2A mean fluorescence intensity 5692 +/- 2032 versus 4525 +/- 1646, P < 0.05). Twelve individuals were treated with pegylated interferon and ribavirin. This resulted in a down-regulation of NKG2A expression on CD56(dim) NK cells. Individuals with a sustained virological response (SVR) had greater numbers of NKG2A-positive, KIR-negative NK cells than those without SVR (27.6 +/- 9.6% NK cells versus 17.6 +/- 5.7, P < 0.02). Our data show that NKG2A expression is dysregulated in chronic HCV infection and that NKG2A-positive NK cells are associated with a beneficial response to pegylated interferon and ribavirin therapy.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Chronic Hepatitis C treatmentIEP 40818079 RGD 
Chronic Hepatitis C treatmentISOKLRC1 (Homo sapiens)40818079; 40818079 RGD 
Chronic Hepatitis C  IEP 40818079; 40818079protein:increased expression:peripheral blood mononuclear cell and natural killer cell (human)RGD 
Chronic Hepatitis C  ISONCR1 (Homo sapiens)40818079; 40818079protein:increased expression:peripheral blood mononuclear cell and natural killer cell (human)RGD 
Chronic Hepatitis C  ISONCR3 (Homo sapiens)40818079; 40818079protein:increased expression:peripheral blood mononuclear cell and natural killer cell (human)RGD 

Gene-Chemical Interaction Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
ribavirin affects expression EXP 40818079Ribavirin co-treated with Interferon alfa-2a affects expression of KLRC1 protein in Natural Killer cellsRGD 
ribavirin affects expression ISOKLRC1 (Homo sapiens)40818079; 40818079Ribavirin co-treated with Interferon alfa-2a affects expression of KLRC1 protein in Natural Killer cellsRGD 

Objects Annotated

Genes (Rattus norvegicus)
Klrc1  (killer cell lectin like receptor C1)
Ncr1  (natural cytotoxicity triggering receptor 1)
Ncr3  (natural cytotoxicity triggering receptor 3)

Genes (Mus musculus)
Klrc1  (killer cell lectin-like receptor subfamily C, member 1)
Ncr1  (natural cytotoxicity triggering receptor 1)
Ncr3-ps  (natural cytotoxicity triggering receptor 3, pseudogene)

Genes (Homo sapiens)
KLRC1  (killer cell lectin like receptor C1)
NCR1  (natural cytotoxicity triggering receptor 1)
NCR3  (natural cytotoxicity triggering receptor 3)


Additional Information