Most gastric cancers (GC) are thought to be caused by Helicobacter pylori ( H. pylori ) infections. However, there is mounting evidence that GC patients with positive H. pylori status have improved prognoses. The H. pylori -induced cellular immune reaction may inhibit cancer. In this study, BALB/c mice were immunized using recombinant plasmids that encode the ureF gene of H. pylori . Purified functional splenic CD3 + T lymphocytes are used to study the anticancer effects in vitro and in vivo . The immunological state of GC patients with ongoing H. pylori infection is mimicked by the H. pylori DNA vaccines, which cause a change in the reaction from Th1 to Th2. Human GC cells grow more slowly when stimulated CD3 + T lymphocytes are used as adoptive infusions because they reduce GC xenograft development in vivo . The more excellent ratios of infiltrating CD8 + /CD4 + T cells, the decreased invasion of regulatory FOXP3 + Treg lymphocytes, and the increased apoptosis brought on by Caspase9/Caspase-3 overexpression and Survivin downregulation may all contribute to the consequences. Our findings suggest that in people with advanced GC, H. pylori pIRES2-DsRed-Express- ureF DNA vaccines may have immunotherapeutic utility.
Keyphrases
- helicobacter pylori
- helicobacter pylori infection
- induced apoptosis
- gas chromatography
- cell free
- circulating tumor
- cell death
- cell cycle arrest
- single molecule
- endothelial cells
- escherichia coli
- mass spectrometry
- signaling pathway
- regulatory t cells
- papillary thyroid
- high resolution
- immune response
- peripheral blood
- dna methylation
- genome wide
- nucleic acid
- type diabetes
- risk assessment
- gene expression
- mesenchymal stem cells
- squamous cell
- pi k akt
- wild type
- childhood cancer