H pylori infection of T-cell-deficient and Ifngr1-/- mice, and transfer of CD4+ T cells to Rag1-/- mice, showed that cagY-mediated loss of T4SS function requires a T-helper 1-mediated immune response.
Recently, polymorphisms in the gene encoding the interferon gamma receptor 1 (IFNGR1) were found to be associated with increased susceptibility to H pylori infection.
Genetic Polymorphisms of CXCL8 (-251) Are Associated with the Susceptibility of Helicobacter pylori Infection Increased the Risk of Inflammation and Gastric Cancer in Thai Gastroduodenal Patients.
The variant genotype of the TLR4 gene polymorphisms might be protective factors for H.pylori infection, while socioeconomic status is an risk factor for H. pylori infection.
ABO (rs505922) and IL1B (rs1143627) may affect H pylori infection susceptibility, and IL1B (rs1143627) may also influence ID risk in infected children.
Association of Helicobacter pylori infection with Toll-like receptor-4Thr399Ile polymorphism increased the risk of peptic ulcer development in North of Iran.
Association of a single nucleotide polymorphism in the TLR2 gene (rs3804099), but not in the TLR4 gene (rs4986790), with Helicobacter pylori infection and peptic ulcer.
The proinflammatory cytokines of TNF-α and IL-1β have been reported to be increased in gastric mucosal surfaces in people with Helicobacter pylori infection.
The proinflammatory cytokines of TNF-α and IL-1β have been reported to be increased in gastric mucosal surfaces in people with Helicobacter pylori infection.
Combination of Helicobacter pylori infection and the interleukin 8 -251 T > A polymorphism, but not the mannose-binding lectin 2 codon 54 G > A polymorphism, might be a risk factor of gastric cancer.
Thus our findings suggest that TLR4rs4986790, rs4986791 and TLR9 rs352140 polymorphisms are potential genetic risk factors influencing the disease susceptibility and clinical manifestation of chronic H. pylori infection in Indian Tamils.
Gastric cancer is closely associated with Helicobacter pylori infection, which stimulates innate immune responses through Toll-like receptors (TLRs), inducing COX-2/PGE2 pathway through nuclear factor-κB activation.