Hepatitis C Virus Core Protein Induces an Anergic State Characterized by Decreased Interleukin-2 Production and Perturbation of Mitogen-Activated Protein Kinase Responses

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Published inJournal of Virology Vol. 79; no. 4; pp. 2230 - 2239
Main Authors SUNDSTRÖM, Sara, OTA, Seisuke, DIMBERG, Lina Y, MASUCCI, Maria G, BERGQVIST, Anders
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 15.02.2005
Subjects
Biological and medical sciences
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Clinical virology
Clonal Anergy
Enzyme Activation
Fundamental and applied biological sciences. Psychology
Hepacivirus
Hepatitis C virus
Humans
Interleukin-2 - biosynthesis
Jurkat Cells
Klinisk virologi
Medical Virology
MEDICIN
Medicin och hälsovetenskap
MEDICINE
medicinsk virologi
Microbiology
Microbiology, immunology, infectious diseases
Mikrobiologi
Mikrobiologi, immunologi, infektionssjukdomar
Miscellaneous
Mitogen-Activated Protein Kinase Kinases - metabolism
Mitogen-Activated Protein Kinases - metabolism
Pathogenesis and Immunity
T-Lymphocytes - drug effects
T-Lymphocytes - pathology
T-Lymphocytes - virology
Tumor Cells, Cultured
Viral Core Proteins - pharmacology
Virologi
Virology
Virus
Interleukin 2
Microbiology
Enzyme
Cytokine
Mitogen-activated protein kinase
Flaviviridae
Hepatitis C virus
Hepacivirus
Protein
Virology
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Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver cirrhosis and hepatocellular carcinoma. Here we demonstrate that the expression of the HCV core (C) protein in stably transfected T cells correlates with a selective reduction of interleukin-2 (IL-2) promoter activity and IL-2 production in response to T-cell receptor triggering, whereas the activation of IL-4, IL-10, gamma interferon, and tumor necrosis factor alpha was moderately increased. This altered cytokine expression profile was associated with a perturbation of mitogen-activated protein (MAP) kinase responses. Extracellular regulated kinase and p38 were constitutively phosphorylated in C-expressing cells, while triggering of the costimulatory c-Jun N-terminal kinase (JNK) signaling cascade and activation of the CD28 response element within the IL-2 promoter appeared to be impaired. The perturbations of MAP kinase phosphorylation could be eliminated by cyclosporine A-mediated inhibition of nuclear factor of activated T cells, suggesting that the inactivation of JNK signaling and hyporesponsiveness to IL-2 induction were downstream consequences of C-induced Ca 2+ flux in a manner that mimics the induction of clonal anergy.
ABSTRACT Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver cirrhosis and hepatocellular carcinoma. Here we demonstrate that the expression of the HCV core (C) protein in stably transfected T cells correlates with a selective reduction of interleukin-2 (IL-2) promoter activity and IL-2 production in response to T-cell receptor triggering, whereas the activation of IL-4, IL-10, gamma interferon, and tumor necrosis factor alpha was moderately increased. This altered cytokine expression profile was associated with a perturbation of mitogen-activated protein (MAP) kinase responses. Extracellular regulated kinase and p38 were constitutively phosphorylated in C-expressing cells, while triggering of the costimulatory c-Jun N-terminal kinase (JNK) signaling cascade and activation of the CD28 response element within the IL-2 promoter appeared to be impaired. The perturbations of MAP kinase phosphorylation could be eliminated by cyclosporine A-mediated inhibition of nuclear factor of activated T cells, suggesting that the inactivation of JNK signaling and hyporesponsiveness to IL-2 induction were downstream consequences of C-induced Ca 2+ flux in a manner that mimics the induction of clonal anergy.
Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver cirrhosis and hepatocellular carcinoma. Here we demonstrate that the expression of the HCV core (C) protein in stably transfected T cells correlates with a selective reduction of interleukin-2 (IL-2) promoter activity and IL-2 production in response to T-cell receptor triggering, whereas the activation of IL-4, IL-10, gamma interferon, and tumor necrosis factor alpha was moderately increased. This altered cytokine expression profile was associated with a perturbation of mitogen-activated protein (MAP) kinase responses. Extracellular regulated kinase and p38 were constitutively phosphorylated in C-expressing cells, while triggering of the costimulatory c-Jun N-terminal kinase (JNK) signaling cascade and activation of the CD28 response element within the IL-2 promoter appeared to be impaired. The perturbations of MAP kinase phosphorylation could be eliminated by cyclosporine A-mediated inhibition of nuclear factor of activated T cells, suggesting that the inactivation of JNK signaling and hyporesponsiveness to IL-2 induction were downstream consequences of C-induced Ca2+ flux in a manner that mimics the induction of clonal anergy.
Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver cirrhosis and hepatocellular carcinoma. Here we demonstrate that the expression of the HCV core (C) protein in stably transfected T cells correlates with a selective reduction of interleukin-2 (IL-2) promoter activity and IL-2 production in response to T-cell receptor triggering, whereas the activation of IL-4, IL-10, gamma interferon, and tumor necrosis factor alpha was moderately increased. This altered cytokine expression profile was associated with a perturbation of mitogen-activated protein (MAP) kinase responses. Extracellular regulated kinase and p38 were constitutively phosphorylated in C-expressing cells, while triggering of the costimulatory c-Jun N-terminal kinase (JNK) signaling cascade and activation of the CD28 response element within the IL-2 promoter appeared to be impaired. The perturbations of MAP kinase phosphorylation could be eliminated by cyclosporine A-mediated inhibition of nuclear factor of activated T cells, suggesting that the inactivation of JNK signaling and hyporesponsiveness to IL-2 induction were downstream consequences of C-induced Ca super(2+) flux in a manner that mimics the induction of clonal anergy.
Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver cirrhosis and hepatocellular carcinoma. Here we demonstrate that the expression of the HCV core (C) protein in stably transfected T cells correlates with a selective reduction of interleukin-2 (IL-2) promoter activity and IL-2 production in response to T-cell receptor triggering, whereas the activation of IL-4, IL-10, gamma interferon, and tumor necrosis factor alpha was moderately increased. This altered cytokine expression profile was associated with a perturbation of mitogen-activated protein (MAP) kinase responses. Extracellular regulated kinase and p38 were constitutively phosphorylated in C-expressing cells, while triggering of the costimulatory c-Jun N-terminal kinase (JNK) signaling cascade and activation of the CD28 response element within the IL-2 promoter appeared to be impaired. The perturbations of MAP kinase phosphorylation could be eliminated by cyclosporine A-mediated inhibition of nuclear factor of activated T cells, suggesting that the inactivation of JNK signaling and hyporesponsiveness to IL-2 induction were downstream consequences of C-induced Ca(2+) flux in a manner that mimics the induction of clonal anergy.
Author Seisuke Ota
Anders Bergqvist
Sara Sundström
Maria G. Masucci
Lina Y. Dimberg
AuthorAffiliation Microbiology and Tumor Biology Centre, Karolinska Institutet, Stockholm, 1 Department of Medical Biochemistry and Microbiology, Biomedical Centre, Uppsala University, Uppsala, Sweden 2
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Keywords Virus
Interleukin 2
Microbiology
Enzyme
Cytokine
Mitogen-activated protein kinase
Flaviviridae
Hepatitis C virus
Hepacivirus
Protein
Virology
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Corresponding author. Mailing address: MTC, Karolinska Institutet, Box 280, SE-171 77 Stockholm, Sweden. Phone: 46-8-52487149. Fax: 46-8-331399. E-mail: anders.bergqvist@mtc.ki.se.
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Snippet Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver...
ABSTRACT Alterations of cytokine responses are thought to favor the establishment of persistent hepatitis C virus (HCV) infections, enhancing the risk of liver...
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StartPage 2230
SubjectTerms Biological and medical sciences
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Clinical virology
Clonal Anergy
Enzyme Activation
Fundamental and applied biological sciences. Psychology
Hepacivirus
Hepatitis C virus
Humans
Interleukin-2 - biosynthesis
Jurkat Cells
Klinisk virologi
Medical Virology
MEDICIN
Medicin och hälsovetenskap
MEDICINE
medicinsk virologi
Microbiology
Microbiology, immunology, infectious diseases
Mikrobiologi
Mikrobiologi, immunologi, infektionssjukdomar
Miscellaneous
Mitogen-Activated Protein Kinase Kinases - metabolism
Mitogen-Activated Protein Kinases - metabolism
Pathogenesis and Immunity
T-Lymphocytes - drug effects
T-Lymphocytes - pathology
T-Lymphocytes - virology
Tumor Cells, Cultured
Viral Core Proteins - pharmacology
Virologi
Virology
Title Hepatitis C Virus Core Protein Induces an Anergic State Characterized by Decreased Interleukin-2 Production and Perturbation of Mitogen-Activated Protein Kinase Responses
URI http://jvi.asm.org/content/79/4/2230.abstract
https://www.ncbi.nlm.nih.gov/pubmed/15681425
https://search.proquest.com/docview/17864037
https://pubmed.ncbi.nlm.nih.gov/PMC546561
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-86667
http://kipublications.ki.se/Default.aspx?queryparsed=id:1948385
Volume 79
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