4.8 Article

Decrease in CD3-negative-CD8dim+ and Vδ2/Vγ9 TcR+ peripheral blood lymphocyte counts, low perforin expression and the impairment of natural killer cell activity is associated with chronic hepatitis C virus infection

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JOURNAL OF HEPATOLOGY
卷 37, 期 4, 页码 514-522

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ELSEVIER SCIENCE BV
DOI: 10.1016/S0168-8278(02)00218-0

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hepatitis C virus; CD3-negative-CD8(+) lymphocytes; gamma/delta T cells; perforin; natural killer cytotoxicity; interferon

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Background/Aims: As chronic hepatitis C virus (HCV) infection is associated with impaired natural killer (NK) cell cytotoxicity, we examined the phenotypes and perforin expression of peripheral blood lymphocytes, as well as the effect of interferon-alpha2b (IFN-alpha2b) therapy. Methods: Thirty-three patients had chronic hepatitis C, and of them 12 had been on IFN-alpha2b treatment. Eleven individuals had been treated earlier with IFN-alpha2b and completely cured, and eight were HCV carriers with persistently normal serum alanine aminotransferase. Three-colour flow cytometry was used to measure the percentage of CD3(+)/(-)CD8 +, CD3 + CD4 +, gammadeltaTcR +, Vdelta2 TcR +, Vgamma9 TcR +, Vdelta1 TcR +, CD3 - CD16 +, CD3 - CD56 +, CD19 + and perforin-positive cells. NK cell activity was assessed by single cell cytotoxic and How cytometric assay. Results: Patients with chronic hepatitis C showed an impaired NK cytotoxicity, decreased percentage of CD3-negative-CD8dim-positive (NK subtype) and Vgamma9N62 TcR + as well as perforin-positive T lymphocytes, compared to controls and to those who were cured from HCV infection. IFN-delta2b increased NK cell cytotoxicity and the percentage of perforin-positive lymphocytes. Conclusions: Our findings suggest that in chronic HCV infection a decreased percentage of CD3(-)CD8 +, Vgamma9N82 TcR + and perforin-positive T cells and simultaneous decreased peripheral NK activity may contribute to the impaired cellular immune response and the chronicity of the disease. (C) 2002 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved.

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