Terrés A M, Pajares J M
Gastroenterology Service, Hospital de la Princesa and Universidad Autónoma de Madrid, Spain.
Am J Gastroenterol. 1998 Apr;93(4):579-83. doi: 10.1111/j.1572-0241.1998.168_b.x.
An immune response occurring in Helicobacter pylori-infected gastric mucosa could have a direct implication for associated pathologies. In the present study we analyzed the expression of the immune activation, proliferation, and phenotype markers by immune cell subpopulations in H. pylori-infected and uninfected gastric samples.
Antral gastric biopsies from both H. pylori-positive and -negative patients were processed by immunohistochemistry; gastric epithelial cells were isolated from biopsy tissue and analyzed by flow cytometry.
Ten of the 13 biopsies that contained follicles were H. pylori positive. Follicular CD69 was expressed mainly by CD4+ T cells and the central core of follicles showed double immunopositivity for the B-cell marker CD19 and transferrin receptor. Also detected was an increase in the percentage of epithelial cells from H. pylori-positive samples expressing HLA-DR and beta2 microglobulin, compared to negative samples (61 +/- 15% vs 9 +/- 9%, p = 0.003 and 93 +/- 7% vs 52 +/- 18%, p = 0.002, respectively), whereas no variation on class I HLA was detected.
These results suggest that chronic H. pylori infection could facilitate the persistence of follicles on which continuous follicular helper T-cell activation could lead to uncontrolled follicular B-cell proliferation. Furthermore, beta2 microglobulin expression by epithelial cells in a nonparallel way to class I HLA may indicate the possibility of nonclassical class I MHC expression on the basal surface of the epithelium.
幽门螺杆菌感染的胃黏膜中发生的免疫反应可能与相关病理状况直接相关。在本研究中,我们分析了幽门螺杆菌感染和未感染的胃样本中免疫细胞亚群的免疫激活、增殖和表型标志物的表达情况。
对幽门螺杆菌阳性和阴性患者的胃窦活检组织进行免疫组织化学处理;从活检组织中分离胃上皮细胞并通过流式细胞术进行分析。
13例含有滤泡的活检组织中有10例幽门螺杆菌呈阳性。滤泡性CD69主要由CD4 + T细胞表达,滤泡的中心核心对B细胞标志物CD19和转铁蛋白受体呈双重免疫阳性。与阴性样本相比,幽门螺杆菌阳性样本中表达HLA - DR和β2微球蛋白的上皮细胞百分比也有所增加(分别为61±15%对9±9%,p = 0.003;93±7%对52±18%,p = 0.002),而未检测到I类HLA的变化。
这些结果表明,慢性幽门螺杆菌感染可能促进滤泡的持续存在,持续的滤泡辅助性T细胞激活可能导致滤泡性B细胞不受控制的增殖。此外,上皮细胞中β2微球蛋白的表达与I类HLA不平行,这可能表明上皮基底面存在非经典I类MHC表达的可能性。