Roles of Plasmacytoid Dendritic Cells in Gastric Cancer

Abstract

Gastric cancer (GC) is the fifth most common neoplasm and the third most deadly cancer in humans worldwide. Helicobacter pylori infection is the most important causative factor of gastric carcinogenesis, and activates host innate and adaptive immune responses. As key constituents of the tumor immune microenvironment, plasmacytoid dendritic cells (pDCs) are increasingly attracting attention owing to their potential roles in immunosuppression. We recently reported that pDCs have vital roles in the development of immunosuppression in GC. Clarifying the contribution of pDCs to the development and progression of GC may lead to improvements in cancer therapy. In this review, we summarize current knowledge regarding immune modulation in GC, especially the roles of pDCs in GC carcinogenesis and treatment strategies.

Keywords: Helicobacter pylori; gastric cancer; immune modulation; plasmacytoid dendritic cells; tumor microenvironment.

Figure 1

Immune modulation in gastric mucosa during inflammation. H. pylori, other bacteria and their products stimulates gastric epithelial cells and recruits immune cells to the site of infection, leading to persistent chronic inflammation. However, pDCs may recruit Treg cells to promote immunosuppression. Treg, regulatory T cell; Th1, T helper cell type 1; Th17, T helper cell type 17; DC, dendritic cell; MΦ, macrophage; pDC, plasmacytoid dendritic cell; IL-10, interleukin 10; TGF-β, transforming growth factor-β.