Helicobacter pylori is a Gram-negative, microaerobic bacterium that colonizes the human gastric mucosa and is significantly associated with the development of chronic gastritis, peptic ulcer, gastric mu-cosa-associated lymphoma, gastric tumors, and gastric polyps. Infection of gastric mucosal cells with H. py-lori can activate nuclear factor-κB signaling pathway, induce interleukin-8 (IL-8) release, recruit antigen-presenting cells (APCs), and stimulate the host to produce innate and adaptive immune responses, resulting in anti-H. pylori effects in the host. However, the bacterium has the ability to manipulate and disrupt the host immune system, not only by modifying its own structure to avoid recognition by the host immune sys-tem, but also by inhibiting the proliferation and maturation of T and B lymphocytes, promoting T cell apop-tosis, affecting the balance of Th17/Treg differentiation, and inducing the formation of immune tolerance. Furthermore, H. pylori can inhibit Th1 cell-mediated immune responses and promote immune escape by taking up cholesterol, disrupting the cholesterol-rich microdomains of gastric mucosal epithelial cells, and blocking the assembly of interferon-γ (IFN-γ), IL-22 and IL-6 receptors. This paper summarized the H. py-lori-related immune response and immune escape in humans, in hopes of providing reference materials for clinical control and immunotherapy of H. pylori infection.