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• W2004016007 abstract "ABSTRACT In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56 + NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro . Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1 + NK cells, including CD56 bright and CD56 dim subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1 − NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection." @default.
• W2004016007 created "2016-06-24" @default.
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• W2004016007 date "2013-11-01" @default.
• W2004016007 modified "2023-10-16" @default.
• W2004016007 title "KLRG1 Negatively Regulates Natural Killer Cell Functions through the Akt Pathway in Individuals with Chronic Hepatitis C Virus Infection" @default.
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• W2004016007 doi "https://doi.org/10.1128/jvi.01515-13" @default.
• W2004016007 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3807337" @default.
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