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再生障碍性贫血患者细胞免疫功能与造血细胞因子的研究
引用本文:王欣,张明珙,宋素琴. 再生障碍性贫血患者细胞免疫功能与造血细胞因子的研究[J]. 中华血液学杂志, 1998, 19(4): 181-183
作者姓名:王欣  张明珙  宋素琴
作者单位:山东医科大学附属医院
摘    要:目的:进一步探讨再生障碍性贫血(再障)的免疫发病机制,阐明细胞免疫、造血细胞因子在再障患者中发生变化的基础与临床意义。方法:用单抗试剂盒,采用改良APAAP法及酶联免疫试剂盒,采用ELISA法对38例再障患者及20名正常人外周血T细胞亚群,HLA-DR抗原表达以及外周血单个核细胞(PBMNC)培养上清诱生G-CSF、IL-6、TNFα、IFNα及IL-8水平进行测定。结果:再障患者外周血CD4细胞减低、CD8细胞增高、CD4/CD8降低或倒置,HLA-DR抗原表达率增高。再障患者PBMNC培养上清中G-CSF阳性率减低,IL-6、TNFα、IFNα及IL-8水平增高。相关分析发现G-CSF与CD4细胞及CD4/CD8呈正相关,而与IFNα呈负相关;IL-6与白细胞数及CD4细胞呈负相关;TNFα与CD8细胞呈正相关而与CD4/CD8呈负相关;IL-8与CD8细胞及HLA-DR呈正相关。结论:细胞免疫功能异常及细胞因子网络失调在再障发病中起一定的作用。

关 键 词:贫血.再生障碍性  T细胞亚群  HLA-DR抗原类  造血细胞生长因子

Study on the cellular immune function and cytokines in aplastic anemia patients
X Wang,M Zhang,S Song. Study on the cellular immune function and cytokines in aplastic anemia patients[J]. Chinese Journal of Hematology, 1998, 19(4): 181-183
Authors:X Wang  M Zhang  S Song
Affiliation:Affiliated Hospital of Shandong Medical University, Jinan 250012.
Abstract:OBJECTIVE: To evaluate the effects of cellular immune function and cytokines on the pathogenesis of aplastic anemia (AA) and its clinical significance. METHODS: T lymphocyte subsets and HLA-DR antigen expression in the peripheral blood cells were assayed, and the levels of G-CSF, IL-6, TNF alpha, IFN alpha and IL-8 in the PBMNC culture supernatants were determined in 38 AA patients and 20 normal control with APAAP and ELISA methods. RESULTS: CD4+ cells, CD4+/CD8+ cells and G-CSF level were lower, and CD8+ cells, HLA-DR+ cells and IL-6, TNF alpha, IFN alpha and IL-8 levels were higher in AA patients than in normal controls. The level of G-CSF was positively correlated with CD4+ cells and CD4+/CD8+ cells and negatively with IFN alpha level. IL-6 level was negatively correlated with WBC count and CD4+ cells. TNF alpha level was positively correlated with CD8+ cells and negatively with CD4+/CD8+ cells. IL-8 level was positively correlated with CD8+ cells and HLA-DR+ cells. CONCLUSION: The cellular immune dysfunction and cytokine aberration participate in the pathogenesis of AA.
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