Abstract: ObjectiveTo investigate the immunological mechanism of mucosa injury in patients with Helicobacter pylori (Hp) positive atrophic gastritis and provided theoretical evidence for new method or targets to eradicate Hp. MethodsMucosa specimen were collected from 40 superficial gastritis patients (20 Hp positive patients and 20 Hp negative patients), and 40 atrophic gastritis patients (20 Hp positive patients and 20 Hp negative patients). The expression of interleukin 17 (IL-17), toll-like receptor 2 (TLR2) and programmed cell death protein 1 (PD-1) was assessed immunohistochemistry. ResultsPatients with Hp positive superficial gastritis showed remarkably higher levels of IL-17 and PD-1 than those with Hp negative superficial gastritis (P<0.05). Patients with Hp positive atrophic gastritis showed remarkably higher levels of IL-17 and PD-1 than those with Hp negative atrophic gastritis (P<0.05). Patients with Hp positive atrophic gastritis showed remarkably higher levels of IL-17 and PD-1 than those with Hp positive superficial gastritis (P<0.05). No statistical difference was found as to TLR2 level in among the groups. ConclusionHp infection can up-regulate the levels of IL-17 and PD-1. The progression of patients with Hp infection is related to high expression of IL-17 and PD-1, which indicated that IL-17 and PD-1 may also cause immunological damage. TLR2 is not involved in immunological responses of Hp infections in the gastric mucosa.