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
- induced apoptosis
- gas chromatography
- helicobacter pylori infection
- cell free
- circulating tumor
- cell death
- cell cycle arrest
- oxidative stress
- endoplasmic reticulum stress
- single molecule
- endothelial cells
- transcription factor
- cell proliferation
- signaling pathway
- escherichia coli
- mass spectrometry
- cell therapy
- type diabetes
- stem cells
- diabetic rats
- adipose tissue
- risk assessment
- squamous cell carcinoma
- multidrug resistant
- tandem mass spectrometry
- nucleic acid
- klebsiella pneumoniae
- cell migration
- circulating tumor cells
- dendritic cells
- insulin resistance