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| CXCL10 and chronic CHC | References |
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| The intrahepatic production of IFN-γ causes the raised CXCL10 and CXCL9 expression and recruits CXCR3-expressing T cells in the hepatic lobule. | [56] |
| CXCR3 ligands are responsible for regional localization of specific lymphocyte subsets in the HCV-infected liver. | [57] |
| Increased expression, in chronic HCV infection, of IFN-α/β-inducible antiviral MxA gene; gene encoding IFN-α/β-inducible p44; gene encoding IFN-α/β/γ-inducible IFI-56 K. | [58] |
| Hepatocytes in inflammatory areas produce CXCL10 either in autoimmune liver diseases or in chronic viral hepatitis. | [59] |
| Hepatic inflammatory activity was associated more strongly with IFN-γ than with CXCL10. | [60] |
| CXCL10 may be induced by HCV within hepatocytes, resulting to be an important factor in the pathogenesis of CHC. | [61] |
| CXCL10 and CXCL9 gene expression in cultured human hepatocyte-derived cells is upregulated by NS5A and core proteins, alone or in combination with cytokines. | [62] |
| Hepatocytes in CHC patients participate in CXCL10 production involving TLR2 and CD44. | [65] |
| CXCL10 and its noncognate receptor, TLR4, are proapoptotic signaling cascades for hepatocytes during liver injury. | [66] |
| Nonparenchymal hepatic cells and immune effector cells were recruited in the site of infection by CXCL10. These cells by secreting type I, II, and III IFNs amplify CXCL10 response during the later stages of acute HCV infection. | [63] |
| Investigations about the mechanisms of CXCL10 induction in hepatocytes by several factors (such as NF-κB and IRF3). Perpetual inflammation and viral persistence could be arisen because of viral proteins that antagonize with these factors and then interfere with the induction of CXCL10. | [64] |
| In the first stage of liver fibrosis, the principal alterations in gene expression affected in particular the IFN-regulated transcriptional network, such as IFN-α/β-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, and MX1) and IFN-γ-inducible genes (CXCL9, CXCL10, and CXCL11). | [67] |
| CXCL10 mRNA expression levels were significantly associated with lobular necroinflammatory grade and HCV genotype 1. | [68] |
| Patients with advanced fibrosis had significantly increased CXCL10 plasma levels. | [69] |
| CXCR3 chemokines are the most strongly expressed chemokines in CHC and presumably have a key role in positioning T cells in the liver. | [70, 71] |
| CXCL10 is an independent biomarker of the recurrence of significant fibrosis after liver transplantation for HCV infection. | [72] |
| Studies reported that in CHC, CXCL10 can be considered a marker of liver fibrosis. | [73–75] |
| HCV-induced CXCL10 can lead to a raised hepatocyte turnover and the development of cirrhosis, fibrosis, and HCC. | [37] |
| Circulating CXCL10 in many HCV patients is enzymatically processed to produce a CXCL10 antagonist form, introducing a role for chemokine antagonism during HCV infection. | [76–78] |
| Serum CXCL10 levels were significantly lower in patients with seronegative occult HCV infection than in patients with chronic hepatitis C. | [79] |
| The single nucleotide polymorphism CXCL10 rs1439490 G/G is positively associated with occult HCV infection in HCV. | [80] |
| High CXCL10 and TNF-α serum levels were observed in patients with hepatitis C-associated cryoglobulinemia (MC+HCV), and in particular, increased CXCL10 levels were significantly associated with the presence of active vasculitis. | [81] |
| In mixed cryoglobulinemia patients, circulating CXCL10 was higher in those with associated autoimmune thyroiditis. | [82] |
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