CrossRefPubMed 39. Angres B, Kim L, Jung R, Gessner R, Tauber R: LI-cadherin gene expression during mouse intestinal development. Dev Dyn 2001, 221:182–193.CrossRefPubMed 40. Schonig K, Schwenk F, Rajewsky K, Bujard H: Stringent doxycycline dependent control of Thiazovivin in vivo CRE recombinase in vivo. Nucleic Acids Res 2002, 30:e134.CrossRefPubMed 41. Ueberham E, Low R, Ueberham U, Schonig K, Bujard H, Gebhardt R: Conditional tetracycline-regulated
expression of TGF-beta1 in liver of transgenic mice leads to reversible intermediary fibrosis. Hepatology 2003, 37:1067–1078.CrossRefPubMed 42. Ueberham E, Arendt E, Starke M, Bittner R, Gebhardt R: Reduction and expansion of the glutamine synthetase expressing zone in livers from tetracycline controlled TGF-beta1 transgenic mice and multiple starved mice. J Hepatol 2004, 41:75–81.CrossRefPubMed 43. Burger HJ, Gebhardt R, Mayer C, Mecke D: Different capacities for amino acid transport in
periportal and perivenous hepatocytes isolated by digitonin/collagenase perfusion. Hepatology 1989, 9:22–28.CrossRefPubMed 44. Franke WW, Schmid E, Kartenbeck J, Mayer D, Hacker HJ, Bannasch Pinometostat cost P, Osborn M, Weber K, Denk H, Wanson JC, Drochmans P: Characterization of the intermediate-sized filaments in liver cells by immunfluorescence and electron microscopy. Biol Cell 1979, 34:99–110. 45. Zhao L, Burt AD: The diffuse stellate cell system. J Mol Histol 2007, 38:53–64.CrossRefPubMed 46. Tobias PS, Ulevitch RJ: Lipopolysaccharide binding protein and CD14 in LPS dependent macrophage activation. Immunobiology 1993, 187:227–232.PubMed Competing interests The authors declare that they have no competing Thymidine kinase interests. Authors’ contributions EU, JB and UU acquired, analysed and interpreted the data. JG made the confocal laser scanning microscopy and edited the figures. EU wrote the first draft of the manuscript and UU and RG co-wrote the final version. All authors have read
and approved the manuscript.”
“Introduction Hepatitis C virus (HCV) is a major cause of chronic liver disease worldwide. The virus causes chronic infection in 80% of acutely HCV-infected patients; a subset of these individuals develop progressive liver injury leading to liver cirrhosis and/or hepatocellular carcinoma [1, 2]. Immune responses to HCV play Cyclopamine important roles at various stages of the infection. There is emerging evidence that the ability of acutely HCV-infected patients to control the primary HCV infection depends on the vigorous cellular immune reaction to the virus . In the chronic phase of infection, immune responses determine the rate of progression of disease, both by limiting viral replication and by contributing to immunopathology. Livers from chronically HCV-infected individuals show T cell infiltration; however, these cells are not HCV specific and are unable to eradicate the virus .