Production of interleukins 10 and 12 by activated peripheral blood monocytes/macrophages in patients suffering from chronic hepatitis C virus infection with respect to the response to interferon and ribavirin treatment

Amaraa, Ravdan; Marecková, H; Urbánek, Petr; Fucíková, T

doi:10.1016/s0165-2478(02)00102-5

Cited by 18 publications

(13 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This not only refers to chronic HCV carriers [16] but also to healthy blood donors [20], indicating a possible linkage between higher IL-12 levels and treatment response [21,22]. However, our data contrast a previous report describing an association between the IL12B 3 0 UTR 1188-A allele and increased IL-12 production [10], a finding which has recently been questioned [23].…”

Section: Discussioncontrasting

confidence: 73%

Influence of interleukin 12B (IL12B) polymorphisms on spontaneous and treatment-induced recovery from hepatitis C virus infection

Müller

Marques

Sarrazin

et al. 2004

Journal of Hepatology

View full text Add to dashboard Cite

Section: Discussioncontrasting

confidence: 73%

Influence of interleukin 12B (IL12B) polymorphisms on spontaneous and treatment-induced recovery from hepatitis C virus infection

Müller

Marques

Sarrazin

et al. 2004

Journal of Hepatology

View full text Add to dashboard Cite

“…Since both basal and IFN-␥-induced LMP2 expression is absolutely dependent on IRF-1, it is not surprising that inhibition of IRF-1 by the core protein also results in suppression of LMP2 expression. Considering that a reduction in the population and specific activity of CTL (2,32,35) have been observed in chronically infected individuals, we speculate that the HCV core protein down-modulation of LMP2 may be partially responsible for these in vivo observations. An analysis of the proteasome composition in HCV patients would, therefore, be very useful.…”

Section: Discussionmentioning

confidence: 73%

Repression of Interferon Regulatory Factor 1 by Hepatitis C Virus Core Protein Results in Inhibition of Antiviral and Immunomodulatory Genes

Ciccaglione

Stellacci

Marcantonio

et al. 2007

J Virol

View full text Add to dashboard Cite

Hepatitis C virus (HCV) proteins are known to interfere at several levels with both innate and adaptive responses of the host. A key target in these effects is the interferon (IFN) signaling pathway. While the effects of nonstructural proteins are well established, the role of structural proteins remains controversial. We investigated the effect of HCV structural proteins on the expression of interferon regulatory factor 1 (IRF-1), a secondary transcription factor of the IFN system responsible for inducing several key antiviral and immunomodulatory genes. We found substantial inhibition of IRF-1 expression in cells expressing the entire HCV replicon. Suppression of IRF-1 synthesis was mainly mediated by the core structural protein and occurred at the transcriptional level. The core protein in turn exerted a transcriptional repression of several interferonstimulated genes, targets of IRF-1, including interleukin-15 (IL-15), IL-12, and low-molecular-mass polypeptide 2. These data recapitulate in a unifying mechanism, i.e., repression of IRF-1 expression, many previously described pathogenetic effects of HCV core protein and suggest that HCV core-induced IRF-1 repression may play a pivotal role in establishing persistent infection by dampening an effective immune response.Infection with hepatitis C virus (HCV) represents the major cause of liver disease, affecting more than 170 million individuals worldwide (26). After a subclinical phase, more than 80% of patients progress to persistent HCV infection, which is the leading cause of chronic liver disease associated with cirrhosis and hepatocellular carcinoma (13). The persistence of the virus in the majority of infected individuals is linked to the ability of HCV to evade and/or antagonize the host immune response at both the local and systemic levels. Accordingly, although hepatocytes are a major target of HCV infection, the virus can also replicate in immune cells, including effector cells (1,11). In this respect, resistance to interferon (IFN) therapy is a hallmark of evolution in persistence, indicating that knocking down the antiviral and immunomodulating effects of IFN is a successful strategy for evading the host immune surveillance (21). The production and secretion of IFN type I is pivotal in inducing a global antiviral state through paracrine IFN production and the subsequent activation of interferon-stimulated genes (ISGs) within the infected cells and in the surrounding tissues (70). The role of IFN in HCV infection is thus crucial (21). Functional genomic analyses from cohorts of human subjects with chronic infection have shown that infection is associated with a gene expression profile marked by ISGs whose level of expression is related to different degrees of liver fibrosis and cirrhosis (67). Similarly, gene expression profiling has demonstrated that acute resolving infections in chimpanzees are associated with high levels of hepatic ISG expression (4).The single-stranded RNA genome of HCV is translated into a polypeptide precursor of 3,010 amino aci...

show abstract

“…Relevant to HCV, HCV-specific IL-10 + CD8 T-cell frequency in the liver correlated inversely to histological activity (16,39). Additionally, changes in serum or Tcell IL-10 levels have been associated with the efficacy of antiviral therapy in some studies (32,34,(40)(41)(42)(43)(44)(45)(46).…”

Section: Discussionmentioning

confidence: 99%

Peripheral virus-specific T-cell interleukin-10 responses develop early in acute hepatitis C infection and become dominant in chronic hepatitis

Kaplan¹,

Ikeda²,

Li³

et al. 2008

Journal of Hepatology

View full text Add to dashboard Cite

show abstract

Production of interleukins 10 and 12 by activated peripheral blood monocytes/macrophages in patients suffering from chronic hepatitis C virus infection with respect to the response to interferon and ribavirin treatment

Cited by 18 publications

References 19 publications

Influence of interleukin 12B (IL12B) polymorphisms on spontaneous and treatment-induced recovery from hepatitis C virus infection

Influence of interleukin 12B (IL12B) polymorphisms on spontaneous and treatment-induced recovery from hepatitis C virus infection

Repression of Interferon Regulatory Factor 1 by Hepatitis C Virus Core Protein Results in Inhibition of Antiviral and Immunomodulatory Genes

Peripheral virus-specific T-cell interleukin-10 responses develop early in acute hepatitis C infection and become dominant in chronic hepatitis

Contact Info

Product

Resources

About