Abstract
Gastric cancer is associated with chronic inflammation and Helicobacter pylori infection. Th17 cells are CD4+ T cells associated with infections and inflammation; but their role and mechanism of induction during carcinogenesis is not understood. Gastric myofibroblasts/fibroblasts (GMF) are abundant class II MHC expressing cells that act as novel antigen presenting cells. Here we have demonstrated the accumulation of Th17 in H. pylori-infected human tissues and in the gastric tumor microenvironment. GMF isolated from human gastric cancer and H. pylori infected tissues co-cultured with CD4+ T cells induced substantially higher levels of Th17 than GMF from normal tissues in an IL-6, TGF-β, and IL-21 dependent manner. Th17 required interaction with class II MHC on GMF for activation and proliferation. These studies suggest that Th17 are induced during both H. pylori infection and gastric cancer in the inflammatory milieu of gastric stroma and may be an important link between inflammation and carcinogenesis.
Highlights
Gastric cancer is the 4th most prevalent cancer with the 2nd highest cancer-related mortality rates worldwide
H. pylori infection and gastric cancer are associated with chronic inflammation, little is known about the role Th17 play in the mucosa during these diseases
We examined the presence of the Th17 using RORc and IL-17A markers in mucosa derived from normal samples, H. pylori infected samples with gastritis, and matched normal and gastric cancer tissues from the same patient
Summary
Gastric cancer is the 4th most prevalent cancer with the 2nd highest cancer-related mortality rates worldwide. The risk of developing gastric cancer is 1 in 115, with a survival rate of only 20–30% for 5 years [1]. Chronic inflammation associated with Helicobacter pylori infection is the number one risk factor for gastric cancer. H. pylori infects over 50% of the world’s population with 1% of those infected going on to develop gastric cancer. An estimated 75% of all gastric cancer cases are associated with H. pylori infection [2]. The carcinogenic potential of H. pylori is driven by the interplay between bacterial virulence factors and the host’s immune responses resulting in chronic inflammation, which in turn leads to tumorigenesis
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