We further found that RIP3 knockdown results in an increase of MDSCs and a decrease of interferon gamma-positive (IFN-γ<sup>+</sup> ) cluster of differentiation 8-positive (CD8<sup>+</sup> ) tumor-infiltrating lymphocytes (IFN-γ<sup>+</sup> CD8<sup>+</sup> T cells) in hepatoma tissues, thus promoting immune escape and HCC growth in immunocompetent mice.
We examined the expression of IFN-gamma-R and IFN-gamma-inducible genes in 44 cases with HCC using real-time reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry.
Conclusion: This work demonstrates that NK cell-derived IFN-γ promotes HCC through the EpCAM-EMT axis in HBs-Tg mice, revealing the importance of innate immunity in pathogenesis of HBV-associated HCC.
T-cell responses were investigated by interferon-gamma (IFN-γ) enzyme-linked immunospot and cytotoxic T lymphocyte (CTL) assays using peripheral blood mononuclear cells (PBMCs) in 47 patients, and tumor-infiltrating lymphocytes in 8 of 47 patients with HCC.
In this study, we thoroughly investigated the effect of IFN-gamma on the susceptibility of one human normal liver cell line and 12 HCC cell lines to Fas-mediated cell death.
Interferon-gamma sensitizes hepatitis B virus-expressing hepatocarcinoma cells to 5-fluorouracil through inhibition of hepatitis B virus-mediated nuclear factor-kappaB activation.
The experiments were performed in 5 groups (phosphate buffered saline/PBS, BMSCs, BMSC-IFN-γ, BMSC-IL-10 and BMSC-IFN-γ-IL-10) and the genetically engineered BMSCs were transplanted into HCC mice.
Combination of intratumoral iNKT cells and IFN-γ is a promising independent predictor for recurrence and survival in HCC, which has a better power to predict HCC patients' outcome compared with intratumoral iNKT cells or IFN-γ alone.
In order to investigate the role of NO in Epo production in Hep3B cells under normoxic (20% O2) conditions, we have studied the effects of interferon-gamma (IFN-gamma) on Epo production.
Moreover, soluble mediators secreted by NKL-IL15 cells decreased HCC cell proliferation; in particular, NKL-IL15-derived TNF-α and IFN-γ induced higher NKG2D ligand expression on target cells and resulted in the increased susceptibility of HCCs to NKL-mediated cytolysis.
No significant difference in the frequency of IL-10 SNP at position -1082 or IFN-γ at position +874T/A was found between chronic HCV genotype 4 and with progression of disease severity in liver cirrhosis or HCC.
For T helper (Th) 1 genes (IFNgamma, IL-6 and IL-12), relative to the putative high-activity genotypes, individual low-activity genotypes were associated with statistically non-significant increases in HCC risk.