The role of toll‐like receptors in immune tolerance induced by Helicobacter pylori infection

Abstract

Helicobacter pylori (H. pylori) is a gram‐negative, microaerobic bacterium that colonizes the gastric mucosa in about half of the world's population. H. pylori infection can lead to various diseases. Chronic infection by H. pylori exposes the gastric mucosa to bacterial components such as lipopolysaccharide (LPS), outer membrane vesicles (OMVs), and several toxic proteins. Infected with H. pylori activates the release of pro‐inflammatory factors and triggers inflammatory responses that damage the gastric mucosa. As the only microorganism that permanently colonizes the human stomach, H. pylori can suppress host immunity to achieve long‐term colonization. Toll‐like receptors (TLRs) play a crucial role in T‐cell activation, promoting innate immune responses and immune tolerance during H. pylori infection. Among the 10 TLRs found in humans, TLR2, TLR4, TLR5, and TLR9 have been thoroughly investigated in relation to H. pylori‐linked immune regulation. In the present review, we provide a comprehensive analysis of the various mechanisms employed by different TLRs in the induction of immune tolerance upon H. pylori infection, which will contribute to the research of pathogenic mechanism of H. pylori.

Cross-talk between Helicobacter pylori and gastric cancer: a scientometric analysis

“…HP not only produces immune tolerance by inhibiting T cell function, but also can modify the structure of LPS to evade the recognition of Toll-like receptors (TLRs) pattern recognition receptor family molecules to achieve the purpose of immune escape ( Peek et al., 2010 ). TLRs act in T cell activation, promoting innate immune response and immune tolerance during HP infection ( Zhang et al., 2023 ), which are considered to be the core defects leading to inflammation and cancer development. HP infection can up-regulate the expression of PD-L1 in GC cells by activating the p38 mitogen-activated protein kinase pathway, inhibiting the proliferation of T cells and inducing the differentiation of naive T cells into Treg cells, thereby avoiding immune surveillance and promoting immune escape that ultimately leads to carcinogenesis ( Deng et al., 2022 ).…”