Heat‐killed <i>Helicobacter pylori</i> upregulates NKG2D ligands expression on gastric adenocarcinoma cells via Toll‐like receptor 4

Abstract

Our data indicate that induction of NKG2DL expression on gastric adenocarcinoma cells by H. pylori promotes an immune response that may ultimately contribute to either gastric tissue damage, as a consequence of persistent activation of immunity, or tumor immune evasion due to chronic NKG2DL expression.