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BukuComparison of Cytotoxic T-Lymphocyte Responses to Hepatitis C Virus Core Protein in Uninfected and Infected Individuals (from Journal of Medical Virology 1999, 58, 239-246)
Bibliografi
Author: Jackson, Margaret ; Smith, Belinda ; Bevitt, Debra J. ; Steward, Michael ; Toms, Geoffrey L. ; Bassendine, Margaret F. ; Diamond, Austin G.
Topik: Dendritic cells; HLA-A*0201; Synthetic peptides; Validation ref - 6
Bahasa: (EN )    
Penerbit: Wiley-Liss, Inc     Tempat Terbit: New York    Tahun Terbit: 1999    
Jenis: Article - diterbitkan di jurnal ilmiah internasional
Fulltext: jackson1999.pdf (117.62KB; 0 download)
Abstract
Cytotoxic T lymphocytes have been implicated in the control of hepatitis C virus (HCV) infection. Recognition by cytotoxic T lymphocytes of epitopes within HCV core protein has been defined previously by in vitro stimulation with synthetic peptides. The aim of this study has been to examine cytotoxic T-lymphocyte responses generated against peptides produced naturally following intracellular processing of viral protein. Antigen-specific cytotoxic T-lymphocyte lines were generated from both HCV uninfected and infected individuals by culturing CD8+ T cells with autologous dendritic cells loaded intracytoplasmically with recombinant HCV core protein. Analysis of the epitopes recognized by core protein-specific cytotoxic T lymphocytes used synthetic peptides that were selected based on their
predicted binding to HLA-A*0201 molecules. Core protein-specific cytotoxic T lymphocytes derived from HCV uninfected and infected individuals were able to lyse autologous target cells pulsed with each of 5 predicted epitopes. Generation of HCV-specific cytotoxic T lymphocytes using dendritic cells as antigen presenting cells provides a method of comparing the potential repertoire of cytotoxic T-lymphocyte responses to the responses that occur in chronically infected individuals. No evidence of a qualitatively different response by patient cytotoxic T lymphocytes was apparent which might explain persistence of the virus.

[validation ref - 6]
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