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.
Furthermore, combinations of CTLA-4 -318 TC/TT and TNF -238 GG/GA; CTLA-4 -318 TC/TT and IL 10 -819 CC; CTLA-4 -318 CC and IL 10 -819 CT/TT in patients with HCC were statistically significant (P < .05).
Unlike liver patients without malignancy and healthy controls, the frequency of checkpoint inhibitor-positive Tregs inversely correlated to age of patients with HCC (PD-L1, p = 0.0080; CTLA-4, p = 0.0029) and corresponded to enhanced numbers of Tregs producing IL-10 and IL-35 (p < 0.05 each).
Hypoxia-inducible gene 2 promotes the immune escape of hepatocellular carcinoma from nature killer cells through the interleukin-10-STAT3 signaling pathway.
The fusion protein had the bispecific ability to target both IL-10 and CD19 molecules in vitro.Intramuscularly (i.m.) injecting mice with pcCD19scFv-IL-10R plasmid inhibited hepatocellular carcinoma growth in vivo.
Following treatment with Foxp3-shRNA, the average tumor volume, ratio of Tregs/CD4<sup>+</sup> T cells and level of IL-10, TGF-β and VEGF significantly decreased, however, the level of IFN-γ and IL-2 significantly increased compared with un-treated HCC mice (P<0.05).
Mechanistically, sunitinib treatment primes the antitumor immune response by significantly decreasing Treg frequency, reducing TGF-β and IL-10 production by Tregs, and also protecting TAS CD8<sup>+</sup> T cells from tumor-induced deletion in the setting of HCC.
The tumor microenvironment was improved in DEX<sub>AFP</sub>-treated HCC mice, demonstrated by significantly more γ-interferon (IFN-γ)-expressing CD8<sup>+</sup> T lymphocytes, elevated levels of IFN-γ and interleukin-2, and fewer CD25<sup>+</sup>Foxp3<sup>+</sup> regulatory T (Treg) cells and decreased levels of interleukin-10 and transforming growth factor-β in tumor sites.
IL-6 and IL-10 were significantly increased in both the HCC and GBC groups, IL-2, IL-6, IL-10, and TNF-<i>α</i> in the cholangiocellular carcinoma group, and IL-2, IL-6, IL-8, and TNF-<i>α</i> in the pancreatic cancer group.
These cells also express programmed death ligand 1 (PD-L1) and interleukin-10, and directly suppress liver cytotoxic CD8<sup>+</sup> T lymphocytes, which prevent emergence of hepatocellular carcinoma and express a limited repertoire of T-cell receptors against tumour-associated antigens.
This meta-analysis was designed to examine the association of three promoter polymorphisms (-592C > A, -819C > T and -1082G > A) in IL-10 gene with the risk for colorectal cancer and hepatocellular carcinoma.
Additionally, the IL-10 -819 (-592) TT (AA) genotype was significantly associated with multiple nodules and HCC severity according to BCLC staging (P = 0.044 and P = 0.025, respectively).
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.
In this study, we investigated the influence of IL-21 on HBV replication based on human hepatoma Huh7.93 cells co-cultured with human peripheral blood mononuclear cells (PBMCs) and the possible correlation among IL-21, interferon-γ, tumour necrosis factor-α and IL-10.
The present study was designed to evaluate the impact of IL-10 (-819/-592) genotypes, haplotypes, mRNA and the protein levels with risk for hepatitis B virus (HBV) related hepatocellular carcinoma (HCC) development in India.
In addition, combination analysis with the Th1 cytokine (IFN-γ, IL-2, IL-12B, TGF-β1) or Th2 cytokine (IL-6, IL-10) genetic polymorphisms by the Kaplan-Meier method and Cox multivariate analysis did not reveal any significant association between OS and RFS of resected HCC patients.
We have measured secretion of hepcidin by primary macrophages and the hepatoma cell line HepG2 stimulated with IL-10, IL-6 and Plasmodium falciparum-infected erythrocytes.