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幽门螺杆菌感染的患儿人类白细胞抗原-DQA1的免疫遗传学分析

Immunogenetic analysis of the human leukocyte antigen DQA1 locus in patients with Helicobacter pylori infection

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【作者】 许春娣奚容平陈舜年杨玉琴范丽安徐家裕

【Author】 XU Chundi, XI Rongping, CHEN Shunnian, et al. Department of Pediatrics, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, China

【机构】 上海第二医科大学瑞金医院儿科上海市免疫研究所

【摘要】 目的 幽门螺杆菌 (Helicobacterpylori,Hp)已被广泛认为是慢性胃炎的主要致病原 ,与消化性溃疡和胃腺癌密切相关 ,但Hp引起人类胃肠病的机制尚不清楚 ,许多研究认为可能与患者Hp菌株的毒力高低有关 ,也有认为与宿主的遗传或环境因素有关。本研究为探讨人类白细胞抗原 DQA1(HLA DQA1)基因位点上是否存在与Hp感染及其相关胃炎的易感基因或抵抗基因 ,研究其与免疫遗传的相关性。方法 采用非同位素标记的聚合酶链反应 序列特异性寡核苷酸探针 (PCR SSO)杂交的方法 ,对 130例慢性胃炎及 85名正常对照儿童作了HLA DQA1等位基因型的检测 ,并同时检查了这些患儿的Hp。结果  85例对照组 ,37例Hp阳性 ,48例Hp阴性。 130例慢性胃炎患儿中 ,85例Hp阳性 ,45例Hp阴性。HLA DQA1 0 3等位基因频率在Hp阳性儿童人群及胃炎患儿均明显低于Hp阴性正常健康儿童等位基因频率 (AF) (35 % ,31%对 48% ,P <0 .0 5 )。此外 ,发现DQA1 0 5 0 1基因频率在Hp阳性人群高于无Hp感染者 (2 7%对 13% .P =0 .0 0 7) ,DQA1 0 10 2基因频率在Hp阳性胃炎组显著低于Hp阴性胃炎组 (10 %对 19% ,P =0 .0 36 )。结论 在HLA DQA1基因位点上 ,Hp阳性儿童及胃炎患儿和Hp阴性正常对照组儿童存在着免疫遗传学的差异 ,HLA DQA1 0 3基因对Hp感染可?

【Abstract】 Objective Helicobacter pylori (Hp)is known to be involved in development of digestive diseases such as peptic ulcer, atrophic gastritis, and gastric cancer. It is supposed that the incidence of these digestive diseases associated with Hp is influenced by virulence factor or the host or environmental factors. To explore the immunogenetic mechanism of association between human leukocyte antigen(HLA) and Hp and associated gastritis to search for the possible existence of susceptibility or resistance gene to the disease. Methods The authors used polymerase chain reaction-sequence specific oligonucleotide (PCR-SSO) labeled by non-radioactive method to study the HLA-DQA1 allelic frequency (AF) distribution of 130 cases with gastritis and 85 normal children (control group). All children were examined for Hp infection. Results Of the 85 controls, 37 were Hp positive (+) and 48 were Hp negative (-). Among the 130 chronic gastritis, 85 were Hp positive(+), 45 were Hp negative(-). The AF of HLA-DQA1*03 was significantly lower in children with Hp infection and children with gastritis than that in control group without Hp infection (AF35 %, 31 % vs. 48%, P < 0.05). Besides, AF of DQA1*0501 was higher in Hp infected than that non-Hp infected children. DQA1*0102 was lower in Hp gastritis than that in non-gastritis cases. Conclusion These results suggest that there may be immunogenetic differences in the HLA-DQA1 locus between Hp (+)children, gastritis patients and Hp (-) healthy controls. HLA-QDA1*03 gene has resistance against Hp infection. Whereas the absence of DQA1*0102 may be a host genetic factor for Hp-associated gastritis.

  • 【文献出处】 中华儿科杂志 ,Chinexe Journal of Pediatrics , 编辑部邮箱 ,2000年12期
  • 【分类号】R392
  • 【被引频次】25
  • 【下载频次】91
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