Helicobacter pylori (H. pylori) is a bacterial pathogen that resides in more than half of the human population and has co-evolved with humans for more than 58,000 years. This bacterium is orally transmitted during childhood and is a key cause of chronic gastritis, peptic ulcers and two malignant cancers including MALT (mucosa-associated lymphoid tissue) lymphoma and adenocarcinoma. Despite the strong innate and adaptive immune responses, H. pylori has a long-term survival in the gastric mucosa. In addition to the virulence factors, survival of H. pylori is strongly influenced by the ability of bacteria to escape, disrupt and manipulate the host immune system. This bacterium can escape from recognition by innate immune receptors via altering its surface molecules. Moreover, H. pylori subverts adaptive immune response by modulation of effector T cell. In this review, we discuss the immune-pathogenicity of H. pylori by focusing on its ability to manipulate the innate and acquired immune responses to increase its survival in the gastric mucosa, leading up to gastrointestinal disorders. We also highlight the mechanisms that resulted to the persistence of H. pylori in gastric mucosa.

幽门螺杆菌（H. pylori）是一种细菌病原体，存在于一半以上的人口中，与人类共同进化了58,000多年。该细菌在儿童时期通过口腔传播，是导致慢性胃炎，消化性溃疡和两种恶性肿瘤（包括MALT（黏膜相关淋巴组织）淋巴瘤和腺癌）的主要原因。尽管有很强的先天性和适应性免疫反应，幽门螺杆菌在胃粘膜中仍能长期存活。除毒力因子外，幽门螺杆菌的存活细菌逃逸，破坏和操纵宿主免疫系统的能力受到强烈影响。这种细菌可以通过改变其表面分子而逃避先天免疫受体的识别。此外，幽门螺杆菌通过调节效应T细胞而破坏了适应性免疫应答。在这篇综述中，我们通过关注幽门螺杆菌操纵先天和后天免疫应答以增加其在胃粘膜中的存活率（导致胃肠道疾病）的能力来讨论幽门螺杆菌的免疫致病性。我们还强调了导致幽门螺杆菌在胃粘膜中持续存在的机制。