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作 者:张晓宇[1] 王乐民[1] 龚朱[1] 梁爱斌[2] 王嫱[1] 宋浩明[1]
机构地区:[1]同济大学附属同济医院心内科,上海200065 [2]同济大学附属同济医院血液科,上海200065
出 处:《上海医学》2009年第7期583-585,共3页Shanghai Medical Journal
基 金:国家自然科学基金资助项目(30570809)
摘 要:目的探讨自然杀伤细胞(NK细胞)在肺血栓栓塞症(PTE)过程中的作用。方法随机入选2007年3—12月同济大学附属同济医院住院的20例PTE患者为PTE组,20例同期入院的年龄、性别与之匹配的非PTE患者为对照组。抽取外周静脉血,分离提取单个核细胞总RNA,应用基因表达谱芯片比较两组NK细胞表面受体mRNA表达的差异。结果共筛选出NK细胞识别受体相关基因mRNA片段18条,PTE组杀伤细胞凝集素样受体(KLR)、杀伤细胞免疫球蛋白样受体(KIR)及自然细胞毒效应受体(NCR)mRNA的表达均低于对照组,其中7/9的KLRmRNA及NCR1mRNA的表达显著下调(P值分别<0.05、0.01)。结论PTE过程中NK细胞的自然杀伤功能受抑制,其介导的固有免疫功能缺陷及免疫调节异常可能是获得性PTE的重要机制之一,为阐明PTE的发病机制提供了新的思路。Objective To assess the role of natural killer cells in the pathogenesis of pulmonary thromboembolism (PTE). Methods Twenty patients with PTE were enrolled in our study and another 20 age- and sex-matched non-PTE patients served as controls. Total RNA was extracted from peripheral mononuclear cells. mRNA microarray was used to assess the differential expression of cell surface receptor mRNAs. Results A total of 18 mRNA fragments associated with surface receptors of NK cells were obtained. The mRNA expression of killer cell lectin-like receptors (KLR), killer cell immunolobulin-like receptors (KIR) and natural cytotoxicity receptors (NCR) in PTE group were lower than that of controls, with significant difference found for NCR1 and 7/9 of K/R (P〈0.05). Conclusion The function of NK cells is inhibited in the pathogenesis of PTE. NK-associated innate immunity defficiency and immunoregulatory abnormality may be one of the important pathological mechanisms of acquired VTE, which provides an evidence for the pathological study of VTE. (Shanghai Med J, 2009, 32= 583- 585)
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