McCracken Vance J, Martin Steven M, Lorenz Robin G
Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL 35294-2170, USA.
Immunol Res. 2005;33(2):183-94. doi: 10.1385/IR:33:2:183.
The bacterium Helicobacter pylori is a major human pathogen and the principal cause of acute and chronic gastritis, gastric and duodenal ulcer disease, and gastric adenocarcinoma. Infection with gastric Helicobacter results in an early infiltration of neutrophils, monocytes, and natural killer cells, followed by an influx of T cells and plasma cells. Although the critical components of this gastric infiltrate that lead to disease are unclear, the Helicobacter felis-infected mouse and other mouse models of Helicobacter-associated gastritis have demonstrated the critical nature of adaptive immunity in the development of gastric epithelial pathology. To further investigate the role of adaptive immunity in this disease, adoptive transfer models of disease have also been utilized. These models clearly demonstrate that it is the host CD4+ T lymphocyte response that is crucial for the development of Helicobacter-associated gastric epithelial changes.
幽门螺杆菌是一种主要的人类病原体，是急慢性胃炎、胃和十二指肠溃疡病以及胃腺癌的主要病因。胃部感染幽门螺杆菌会导致中性粒细胞、单核细胞和自然杀伤细胞早期浸润，随后T细胞和浆细胞涌入。虽然导致疾病的这种胃部浸润的关键成分尚不清楚，但感染猫幽门螺杆菌的小鼠和其他幽门螺杆菌相关性胃炎的小鼠模型已证明适应性免疫在胃上皮病理发展中的关键性质。为了进一步研究适应性免疫在这种疾病中的作用，还利用了疾病的过继转移模型。这些模型清楚地表明，宿主CD4 + T淋巴细胞反应对于幽门螺杆菌相关性胃上皮变化的发展至关重要。
