Abstract
In this study, the functions and mechanisms of γ δ T cells were analyzed in patients infected with Helicobacter pylori. Peripheral blood was collected from gastritis patients in the Gastroenterology Department of Ningbo No. 2 Hospital. Preliminary analyses revealed 24 H. pylori-positive and 17 H. pylori-negative patients. The wild-type and γ δ T knockout mice were infected with cultured H. pylori cells (obtained from the H. pylori-positive patients). H. pylori in mice was quantified by polymerase chain reaction; gastritis was confirmed by hematoxylin and eosin staining. The TCR-δ(-/-) mice were treated with vein adoptive immunotherapy 24 h prior to H. pylori inoculation; the same method was used to detect the extent of gastritis and bacterial colonization. The γ δ T knockout mice showed high levels of H. pylori infection than the wild-type mice; in addition, the knockout mice showed severe disease pathology. γ δ T knockout mice also displayed increased matrix metalloproteinase-9 (MMP-9) and decreased MMP-7 expression in the gastric mucosa. γ δ T cells play a protective role in patients infected with H. pylori. γ δ T cell [responsible for the production of interleukin-17 (IL-17) and IL-22] expression was increased in H. pylori-positive patients, indicating statistical significance. However, there was no significant difference in interferon-gamma + γ δ T expression between the positive and negative patients. This study demonstrated the probable involvement of γ δ T cells in the immune response of an organism, via the secretion of IL-17 and IL-22.