Helicobacter pylori, the most common gastric infection in the world, causes gastritis, peptic ulcers, and gastric cancer. Innate and adaptive immune responses are induced after H. pylori infection. However, it achieves long-term colonization through immune evasion. Understanding the mechanisms of inflammation and immunity induced by H. pylori is crucial for developing preventive and therapeutic vaccines. This review captures the major advancements in H. pylori-induced inflammation, immunity, and vaccine development from April 2023 to March 2024. Several studies have revealed new regulators (CDK1 and NOD1) of H. pylori-induced inflammation through NF-kB and non-NF-kB pathways and participation of H. pylori CagA and HtrA. More antimicrobial agents are found to have protective functions by ROS, neutrophil, and NK cell activation. TINAGL1 is reported to negatively modulate DCs and Th1 cells by H. pylori infection in an IL-1β dependent way. Moreover, CD4+IL-17A+FOXP3+ T cells show a proinflammatory function modulated by DCs and IL-6. H. pylori vaccine studies focus on the in-silico design, construction, and in vitro and in vivo evaluation of new vaccine candidates with different strategies. These studies demonstrate promising immunogenicity and efficacy results, underscoring the potential for future vaccine development.