Hepatitis B e antigen was negative in 25% of the children who belonged to groups 1 and 3 and in 27% of the children treated with interferon gamma only.
Interferon-gamma sensitizes hepatitis B virus-expressing hepatocarcinoma cells to 5-fluorouracil through inhibition of hepatitis B virus-mediated nuclear factor-kappaB activation.
Association of interferon-gamma induced protein 10 promoter polymorphisms with the disease progression of hepatitis B virus infection in Chinese Han population.
CD56<sup>bright</sup> NK cells of chronic HBV patients differed in their ability to produce IFN-γ between the clinical phases pre- and post-HBeAg seroconversion.
CTLA4 +49GG genotype was associated to lower TNF-α and IFN-γ levels in patients with chronic HBV infection but this association was diminished by haplotype formation with -318C/T alleles, indicating that the influence of CTLA4 -318C/T and +49A/G polymorphisms on the susceptibility and disease progress of chronic HBV infection may not be effectuated by affecting TNF-α and IFN-γ secretion.
CXCR5<sup>+</sup>CD8<sup>+</sup>T cells are partially exhausted while possess a more potent antiviral activity through producing high levels of HBV-specific IFN-γ and IL-21 in chronic HBV infection.
Cytokines such as TNF-alpha and interferon gamma (IFN-gamma) are important for the elimination of infected hepatocytes during acute hepatitis B virus (HBV) infection.
Detection of Helicobacter pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, pancreatic carcinoma and a cytokine pattern characterised by high interleukin (IL)-10, low/absent interferon-γ and decreased IL-17A concentrations (p < 10(-3)).
Furthermore, we found that these cells could suppress hepatitis B virus-specific CD8(+) T cell response, including reduced proliferation and IFN-γ production, and inhibit degranulation of CD8(+) T cells, including reduced production of granzyme B and perforin.
HBV viral loads, genotypes, precore and basal core promotor mutations, serum hepatitis B surface antigen (HBsAg) and interferon-gamma inducible protein 10 (IP-10) levels as well as four SNPs of IL28B were determined.
Here, we investigated the role of the early activation marker, CD69 and effector cytokines, granzyme B (GrB) and IFN-γ in the exhaustion of innate-like TCR Vα7.2<sup>+</sup>CD4<sup>+</sup>T cells, in 15 individuals with chronic HBV (CHB) infection where six were HBV DNA<sup>+</sup> and nine were HBV DNA<sup>-</sup>.
In addition, the expression of IFN-γ and PD-L1 in the colon was found to be up-regulated early in mice with acute HBV infection, whereas the expression of PD-L1 in the colon of mice with chronic HBV infection was up-regulated later.
In particular, tumor necrosis factor (TNF) and interferon-gamma (IFN-γ) have critical functions in non-cytopathic elimination of hepatitis B virus (HBV) in hepatocytes.
In summary, high-IFNG-producing alleles in intron 1 of the IFNG locus are associated with high [tsIgE] in asthmatic children from Niue and with natural immunity to the HBV in Polynesian women.