Abstract

Dysregulation of the immune system plays a critical role in driving gastric tumorigenesis, as evidenced by the established link between chronic gastric inflammation triggered by infection with gastric pathogens (i.e., Helicobacter pylori, Epstein–Barr virus) and the onset of gastric cancer. Innate immunity is the first line of host defense against invading microbes and is a source of immunomodulatory factors that can shape the course of gastric tumorigenesis. Innate immune responses are orchestrated by pattern recognition receptors, which comprise several superfamilies, namely, Toll-like receptors, NOD-like receptors, RIG-I-like receptors, C-type lectin receptors, and AIM2-like receptors. Recently, it has emerged that pattern recognition receptors not only coordinate inflammatory responses in immune cells, but also direct pro-tumorigenic cellular processes (e.g., proliferation) in non-immune cells, such as epithelial cells. In this chapter, we will discuss recent advancements on the diverse role of innate immune pattern recognition receptors in gastric cancer that have underpinned their potential targeting as drivers of disease pathogenesis.

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