Immune evasion strategies used by Helicobacter pylori

Figure 1 Helicobacter pylori uses gastric epithelial cells as a mediator to inhibit T cell function. Upon binding to an unknown receptor on GEC Helicobacter pylori translocate a hypothetical protein, which causes induction of B7-H1 on GEC. Induction of T cell co-inhibitory molecule B7-H1 further inhibits CD4⁺ T cell proliferation and effector function. It also facilitates induction of T_reg cells from naïve CD4⁺ T cells. This mechanism helps to establish a chronic infection.

Figure 2 Helicobacter pylori mediated downregulation of B7-H2 on gastric epithelial cell inhibits Th17 cell development and facilitates bacterial persistence. Helicobacter pylori T4SS interacts with host receptor integrin α5β1 and translocate effector protein CagA. CagA activates mTOR/p70 S6 kinase pathway and downregulates T cell co-stimulatory molecule B7-H2 expression on GEC. Decreased B7-H2/ICOS signaling further inhibits Th17 cell development from naïve CD4⁺ T cells and Th17 cell mediated bacterial clearance.