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)).
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.
Association of interferon-gamma induced protein 10 promoter polymorphisms with the disease progression of hepatitis B virus infection in Chinese Han population.
Vaccine-specific responses remained stable in the vaccine group, whereas in the control group the percentage of patients with HBV-specific IFN-γ-producing T cells decreased over time.
Less proliferation and lower levels of IL-2 and IFN- γ were also observed in the patient group compared with the control group (P < 0.05).These data suggest that HBV DNA infected and integrated into the BM HSCs from patients with chronic HBV infection and that these BM HSCs generated defective T cells.
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.
The results indicated a statistically significant association between the IFN-γ+874T/A polymorphism and hepatitis virus-related diseases in a recessive gene model (AA vs. TT+TA: OR=1.350, 95% CI=1.101-1.657, P=0.004, I2%=54.3, and PQ=0.001 for heterogeneity), especially in Asians (OR=1.407, 95% CI=1.035-1.911, P=0.029, I2%=61.9, and PQ=0.005 for heterogeneity) and hepatitis B virus (HBV)-related disease (OR=1.486, 95% CI=1.195-1.849, P=0.000, I2%=40.4, and PQ=0.053 for heterogeneity).
Overall, the current study reveals that NK cells, especially DX5(+)CD49a(-) conventional NK cells, promote the antiviral activity of CD8(+) T cell responses via secreting IFN-γ in a mouse model mimicking acute HBV infection.
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.
Levels of HBV DNA and cccDNA in group 5 were lower when compared with those in group 3 or group 4, with a significant difference observed at 48 h. The secretion of interferon‑γ was negatively correlated with the level of HBV DNA, whereas secretion of interleukin (IL)‑10 and IL‑22 were positively correlated with the level of HBV DNA.
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>.
Unresponsiveness to Hepatitis B virus (HBV) vaccine has been associated with interleukins involved with Th1 functioning including Interleukin-8 (IL-18) and Interferon-γ (IFN-γ).
When IFNγ release was considered as readout depicting the hepatitis B vaccination status, the according assay reached a diagnostic sensitivity of 61% without, but of 76% with additional CpG oligonucleotide stimulation at a diagnostic specificity of 90%.
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.