Expression of CCL21 by EBV-associated gastric carcinoma cells protects CD8+CCR7+ T lymphocytes from apoptosis via the mitochondria-mediated pathway

Summary About 10% of gastric carcinomas are associated with Epstein–Barr virus (EBV), which are defined as EBV-associated gastric carcinomas (EBVaGCs). EBVaGCs are usually accompanied by massive lymphocytes infiltration, among which CD8 + T cells are predominant. To date, the apoptosis of the infiltrating CD8 + T cells in EBVaGC has not been investigated. In the present study, we assessed the immunophenotype and apoptosis of tumour infiltrating lymphocytes (TILs) in both EBVaGC and EBV-negative gastric carcinoma (EBVnGC). We found that CD8 + CCR7 + T lymphocytes were increased in EBVaGC compared to EBVnGC [60.53 ± 28.41/high power fields (HPF) vs 19.63 ± 15.97/HPF; p p p + CCR7 + T lymphocytes from apoptosis. Furthermore, the up-regulation of Bcl-2 contributed to the inhibition of apoptosis in CD8 + CCR7 + T cells. Collectively, these findings suggest that expression of CCL21 by EBVaGC cells protects CD8 + CCR7 + T lymphocytes from apoptosis via the mitochondria-mediated pathway. To our best knowledge, this is the first study to investigate the apoptosis of CD8 + T cells in EBVaGC.