**1. Introduction**

*Helicobacter pylori* (*H. pylori*) is one of the most common infections in humans [1–3]. The microorganism had infected humans for 30,000 years ago and has developed extensive adaptations to survive [2, 4, 5]. Approximately, *H. pylori* infects the stomach of half of the human population globally [3, 6, 7]. Besides residing in the stomach, abundant *H. pylori* are also detected in the oral cavity [8]. The colonization is suspected to be started in the childhood period [2, 4, 7] and maybe persisted for decades or life [2, 4]. The presence of spiral microorganisms resembling *H. pylori* had been identified in the stomachs of the animal during the late nineteenth and early twentieth centuries. Similar spiral bacteria were then isolated in humans, particularly those suffering from peptic ulcer disease or gastric cancer. Previously, the microorganism was named 'Campylobacter-like organism', 'gastric Campylobacterlike organism', '*Campylobacter pyloridi*s', or '*Campylobacter pylori'*. The fact that this microorganism is different from members of the genus Campylobacter changes the

name to *H. pylori* [9]. The relationship between this microorganism and peptic ulcer disease was established in 1983 [10]. This microorganism causes a wide spectrum of diseases, such as chronic gastritis, peptic ulcer, gastric adenocarcinoma, and mucosaassociated lymphoid tissue lymphoma [6, 7]. In initial reports from all over the world in the first decade after the discovery of *H. pylori*, approximately 95% of duodenal ulcers and 85% of gastric ulcers occurred in the presence of *H. pylori* infection [9]. The World Health Organization has classified H. pylori as a class I carcinogen due to its epidemiological link with gastric malignancy [2, 3, 10]. However in some cases, the presence of *H. pylori* infection is asymptomatic [3, 7, 11]. There is a hypothesis suggesting the role of immune response in the pathogenesis of infection. The immune response toward the infection is ineffective, causing persistent microorganisms and inflammation [6]. In this review, we discuss the host immune response toward *H. pylori* infection in association with disease chronicity and vaccine development.
