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机构地区:[1]贵阳医学院附属医院口腔内科,贵阳550004 [2]佛山市南海区第二人民医院口腔科,佛山528251 [3]兴义市人民医院口腔科,兴义562400
出 处:《国际口腔医学杂志》2013年第5期568-571,共4页International Journal of Stomatology
基 金:贵州省自然科学基金资助项目(黔科合J字[2010]2165)
摘 要:目的探讨T-bet、GATA-3和Foxp3在复发性阿弗他溃疡(RAU)发病机制中的作用及意义。方法选择RAU患者33例及健康对照30例,采用逆转录聚合酶链反应技术检测患者溃疡发作期外周血单个核细胞(PBMC)中T-bet、GATA-3和Foxp3 mRNA的表达水平,并分析其与RAU免疫功能之间的关系。结果 RAU患者的CD4、CD4/8、T+B+NK细胞含量低于正常值(P<0.01),免疫球蛋白(Ig)A低于正常值(P<0.05),而IgM、血清总补体活性高于正常值(P<0.05)。RAU患者PBMC中T-bet mRNA、T-bet/GATA-3比值、Foxp3 mRNA低于对照组(P<0.01),GATA-3 mRNA高于对照组(P<0.05);Foxp3表达与T-bet/GATA-3比值之间存在正相关关系(r=0.404,P=0.02)。结论 RAU患者大多存在细胞免疫降低和体液免疫紊乱的问题;其溃疡发作期PBMC中GATA-3表达上升,T-bet表达下降,促进了辅助性T细胞(Th)2优势应答,可能是导致RAU患者免疫功能紊乱的原因之一;而调节性T细胞的数量减少及功能低下,这可能与RAU患者Th1/Th2细胞失衡有关。Objective To elucidate the underlying role of T-bet, GATA-3, and Foxp3 in the immune etiology of human with recurrent aphthous ulcer(RAU). Methods Peripheral blood mononuclear cells(PBMCs) were isolated by density gradient centrifugation from 33 cases of RAU and 30 cases of healthy controls. The expression levels of T-bet, GATA-3, and Foxp3 mRNA in PBMCs were investigated by reverse transcription-polymerase chain reaction. The cellular and humoral immune status of patients with RAU was investigated by flow cytometry and enzyme-linked immunosorbent assay. Results CD4, CD4/CD8, T+B+NK cells were significantly lower in the RAU group than in the control group(P〈0.01). Immunoglobulin(Ig) A was lower in the RAU group than in the control group(P〈0.05). IgM and 50% hemolytic complement were significantly higher in the RAU group than in the control group(P〈0.05). The expression level of T-bet mRNA and Foxp3 mRNA, the ratio of T-beffGATA-3 in the RAU group were lower than that in the control group(P〈0.01). Meanwhile, the expression level of GATA-3 mRNA in the RAU group was higher than that in the control group(P〈0.05). A positive correlation was detected between Foxp3 mRNA level and T-bet/GATA-3 ratio(r=0.404, P=0.02). Conclusion Most RAU patients have immune cells reduced and humoral immune disorder. The increased expression of GATA-3 and decreased expression of T-bet might be one of the mechanisms of T helper cell(Th)l/Th2 imbalance in RAU, accounting for the abnormal immune function in patients with RAU. The decrease in regulatory T cells might be a contributing factor toward Thl/Th2 imbalance in RAU.
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