Christian Korner

Summary

Affiliation: University of Bonn
Country: Germany

Publications

  1. doi Effects of HCV co-infection on apoptosis of CD4+ T-cells in HIV-positive patients
    Christian Korner
    Department of Internal Medicine I, University of Bonn, Germany, Sigmund Freud Str 25, Bonn 53127, Germany
    Clin Sci (Lond) 116:861-70. 2009
  2. doi Hepatitis C coinfection enhances sensitization of CD4(+) T-cells towards Fas-induced apoptosis in viraemic and HAART-controlled HIV-1-positive patients
    Christian Korner
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Antivir Ther 16:1047-55. 2011
  3. doi The CXCL1 rs4074 A allele is associated with enhanced CXCL1 responses to TLR2 ligands and predisposes to cirrhosis in HCV genotype 1-infected Caucasian patients
    Hans Dieter Nischalke
    Department of Internal Medicine I, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    J Hepatol 56:758-64. 2012
  4. pmc TRAIL receptor I (DR4) polymorphisms C626G and A683C are associated with an increased risk for hepatocellular carcinoma (HCC) in HCV-infected patients
    Christian Korner
    Department of Internal Medicine I, University of Bonn, Sigmund Freud Str, 25, 53127 Bonn, Germany
    BMC Cancer 12:85. 2012
  5. doi Natural killer p46High expression defines a natural killer cell subset that is potentially involved in control of hepatitis C virus replication and modulation of liver fibrosis
    Benjamin Kramer
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Hepatology 56:1201-13. 2012
  6. doi The toll-like receptor 2 (TLR2) -196 to -174 del/ins polymorphism affects viral loads and susceptibility to hepatocellular carcinoma in chronic hepatitis C
    Hans Dieter Nischalke
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Int J Cancer 130:1470-5. 2012
  7. pmc The CXCR3(+)CD56Bright phenotype characterizes a distinct NK cell subset with anti-fibrotic potential that shows dys-regulated activity in hepatitis C
    Marianne Eisenhardt
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    PLoS ONE 7:e38846. 2012
  8. ncbi An effective interferon-gamma-mediated inhibition of hepatitis C virus replication by natural killer cells is associated with spontaneous clearance of acute hepatitis C in human immunodeficiency virus-positive patients
    Pavlos Kokordelis
    Department of Internal Medicine I, University of Bonn, Bonn, Germany German Center for Infection research DZIF, Bonn, Germany
    Hepatology 59:814-27. 2014
  9. doi Hepatitis C virus core protein induces fibrogenic actions of hepatic stellate cells via toll-like receptor 2
    Martin Coenen
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Lab Invest 91:1375-82. 2011
  10. doi NK cells from HCV-infected patients effectively induce apoptosis of activated primary human hepatic stellate cells in a TRAIL-, FasL- and NKG2D-dependent manner
    Andreas Glässner
    Department of Internal Medicine I, University of Bonn, Germany
    Lab Invest 92:967-77. 2012

Collaborators

Detail Information

Publications16

  1. doi Effects of HCV co-infection on apoptosis of CD4+ T-cells in HIV-positive patients
    Christian Korner
    Department of Internal Medicine I, University of Bonn, Germany, Sigmund Freud Str 25, Bonn 53127, Germany
    Clin Sci (Lond) 116:861-70. 2009
    ..The results of the present study suggest that HCV co-infection sensitizes CD4+ T-cells towards apoptosis in untreated HIV-positive patients. However, this effect is rapidly lost under effective antiretroviral therapy...
  2. doi Hepatitis C coinfection enhances sensitization of CD4(+) T-cells towards Fas-induced apoptosis in viraemic and HAART-controlled HIV-1-positive patients
    Christian Korner
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Antivir Ther 16:1047-55. 2011
    ..Since this effect might be attributed to changes in receptor-induced apoptosis, we studied expression and function of Fas ligand (FasL) and its death receptor Fas on CD4(+) T-cells in HIV/HCV coinfection...
  3. doi The CXCL1 rs4074 A allele is associated with enhanced CXCL1 responses to TLR2 ligands and predisposes to cirrhosis in HCV genotype 1-infected Caucasian patients
    Hans Dieter Nischalke
    Department of Internal Medicine I, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    J Hepatol 56:758-64. 2012
    ..Thus, CXCL1 might contribute to HSC activation and fibrogenesis. Here, we investigated whether the CXCL1 rs4074 polymorphism affects CXCL1 expression and progression of chronic hepatitis C virus (HCV) infection towards cirrhosis...
  4. pmc TRAIL receptor I (DR4) polymorphisms C626G and A683C are associated with an increased risk for hepatocellular carcinoma (HCC) in HCV-infected patients
    Christian Korner
    Department of Internal Medicine I, University of Bonn, Sigmund Freud Str, 25, 53127 Bonn, Germany
    BMC Cancer 12:85. 2012
    ....
  5. doi Natural killer p46High expression defines a natural killer cell subset that is potentially involved in control of hepatitis C virus replication and modulation of liver fibrosis
    Benjamin Kramer
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Hepatology 56:1201-13. 2012
    ..Conclusions: NKp46(High) expression defines a specific NK-cell subset that may be involved in both the suppression of HCV replication and HCV-associated liver damage underpinning the role of NK cells in the immunopathogenesis of HCV...
  6. doi The toll-like receptor 2 (TLR2) -196 to -174 del/ins polymorphism affects viral loads and susceptibility to hepatocellular carcinoma in chronic hepatitis C
    Hans Dieter Nischalke
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Int J Cancer 130:1470-5. 2012
    ..05). Our data suggest the TLR2 -196 to -174 del allele to affect HCV viral loads and to increase the risk for HCC in HCV genotype1-infected patients...
  7. pmc The CXCR3(+)CD56Bright phenotype characterizes a distinct NK cell subset with anti-fibrotic potential that shows dys-regulated activity in hepatitis C
    Marianne Eisenhardt
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    PLoS ONE 7:e38846. 2012
    ..Here, we analyzed phenotype and function of CXCR3 expressing NK cells in chronic hepatitis C...
  8. ncbi An effective interferon-gamma-mediated inhibition of hepatitis C virus replication by natural killer cells is associated with spontaneous clearance of acute hepatitis C in human immunodeficiency virus-positive patients
    Pavlos Kokordelis
    Department of Internal Medicine I, University of Bonn, Bonn, Germany German Center for Infection research DZIF, Bonn, Germany
    Hepatology 59:814-27. 2014
    ..Conclusion: Our data suggest a strong IFN-γ-mediated antiviral NK cell response to be associated with a self-limited course of AHC in HIV(+) patients...
  9. doi Hepatitis C virus core protein induces fibrogenic actions of hepatic stellate cells via toll-like receptor 2
    Martin Coenen
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Lab Invest 91:1375-82. 2011
    ..Manipulating the TLR2 pathway may thus provide a new approach for antifibrotic therapies in HCV infection...
  10. doi NK cells from HCV-infected patients effectively induce apoptosis of activated primary human hepatic stellate cells in a TRAIL-, FasL- and NKG2D-dependent manner
    Andreas Glässner
    Department of Internal Medicine I, University of Bonn, Germany
    Lab Invest 92:967-77. 2012
    ..Here we demonstrate that NK cells from HCV-infected patients are highly efficient in inducing apoptosis of activated HSCs. Thus, NK cells may have an important anti-fibrotic role in chronic hepatitis C...
  11. doi Atorvastatin inhibits proliferation and apoptosis, but induces senescence in hepatic myofibroblasts and thereby attenuates hepatic fibrosis in rats
    Sabine Klein
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Lab Invest 92:1440-50. 2012
    ..Atorvastatin elicits similiar effects on MFB as previously seen in vivo: it decreases MFB turnover and fibrogenesis. We suggest that a further mechanism explaining these effects is senescence of cells...
  12. pmc The PNPLA3 rs738409 148M/M genotype is a risk factor for liver cancer in alcoholic cirrhosis but shows no or weak association in hepatitis C cirrhosis
    Hans Dieter Nischalke
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    PLoS ONE 6:e27087. 2011
    ..I148M, rs738409) has recently been identified as a susceptibility factor for liver damage in steatohepatitis. Here, we studied whether the PNPLA3 rs738409 polymorphism also affects predisposition to hepatocellular carcinoma (HCC)...
  13. doi Regulation of NK cell trafficking by CD81
    Benjamin Kramer
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Eur J Immunol 39:3447-58. 2009
    ..Thus, our data suggest that the tetraspanin CD81 is importantly involved in the regulation of NK cell recruitment...
  14. ncbi The HLA-E(R)/HLA-E(R) genotype affects the natural course of hepatitis C virus (HCV) infection and is associated with HLA-E-restricted recognition of an HCV-derived peptide by interferon-gamma-secreting human CD8(+) T cells
    Daniela Schulte
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    J Infect Dis 200:1397-401. 2009
    ..038). Moreover, we found that the HLA-E(R) allelic variant confers protection against chronic infection with HCV genotypes 2 and 3. Taken together, our data indicate an important immunomodulating function of HLA-E in hepatitis C...
  15. pmc Role of the NK cell-activating receptor CRACC in periodontitis
    Benjamin Kramer
    Department of Medicine I, University of Bonn, Bonn, Germany
    Infect Immun 81:690-6. 2013
    ....
  16. doi Hepatic and HSC-specific sorafenib effects in rats with established secondary biliary cirrhosis
    Martin Hennenberg
    Department of Internal Medicine I, University of Bonn, Bonn, Germany
    Lab Invest 91:241-51. 2011
    ..This leads to the decrease in intrahepatic vascular resistance, but also to liver damage in the dosage we used. Therefore, any translation to portal hypertensive patients who may profit from sorafenib should be done with particular care...