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作 者:熊克宫[1] 陈丽芳[1] 魏大海[1] 孔金峰[1] 孙芳[1] 林太杰[1] 柯坤宇[1]
机构地区:[1]福建省福州市传染病医院肝病科十一区,福州350001
出 处:《海峡药学》2016年第2期242-245,共4页Strait Pharmaceutical Journal
基 金:福州市卫生系统科技计划项目(2014-S-w21)
摘 要:目的研究自身免疫性肝炎(AIH)患者外周血CD4+、CD8+T细胞表面程序性死亡受体1(PD-1)的表达,并探讨其与肝功能指标的相关性。方法收集43例AIH患者(包括活动期31例和缓解期12例),并选择18例健康体检者为对照组。采用流式细胞术检测外周血CD4+、CD8+T细胞表达PD-1的细胞百分比。结果 AIH组外周血CD4+、CD8+T细胞表达PD-1的细胞百分比(分别为7.36±4.45%、6.71±3.84%)显著高于对照组(分别为3.78±2.32%、3.47±2.18%)(P均<0.05);AIH活动期组外周血CD4+、CD8+T细胞表达PD-1的细胞百分比(分别为8.73±6.81%、7.44±2.75%)明显高于缓解期组(分别为5.42±2.14%、4.82±2.04%)和对照组(分别为3.78±2.32%、3.47±2.18%)(P均<0.05),且缓解期组高于对照组(P<0.05)。AIH患者外周血CD4+、CD8+T细胞PD-1表达与TBIL、ALT、AST及Ig G水平均成正相关关系(r分别为0.781、0.887、0.825、0.893,P均<0.05)。结论 AIH患者外周血CD4+、CD8+T细胞表面PD-1表达上调,且与肝功能指标成正相关,提示PD-1可能在AIH的发生及发展中发挥重要作用。OBJECTIVE To investigate the percentage of programmed cell death receptor 1( PD-1) on peripheral blood CD4+,CD8+T cells and explore the correlation with liver liver function indicators in patients with autoimmune hepatitis( AIH). METHODS The percentages of PD-1 on CD4+,CD8+T lymphocytesin peripheral blood of patients with AIH( n = 43) and healthy controls( n = 18) was determined by flow cytometry. RESULTS We found that the percentages of PD-1 on CD4+,CD8+T lymphocytesin peripheral blood of patients with AIH( 7. 36 ± 4. 45%,6. 71 ± 3. 84%,respectively) were higher than the healthy controls( 3. 78 ± 2. 32%,3. 47 ± 2. 18%,respectively)( all P 0. 05). The percentages of PD-1 on CD4+,CD8+T lymphocytes peripheral blood in activity stage( 8. 73 ±6. 81%,7. 44 ± 2. 75%,respectively),remission stage( 5. 42 ± 2. 14%,4. 82 ± 2. 04%,respectively) and the control group( 3. 78 ± 2. 32%,3. 47 ± 2. 18%,respectively) were gradually decline. Correlation analysis showed there was significant correlation between the proportion of peripheral blood CD4+,CD8+T cells expressed PD-1 in AIH and TBIL,ALT,AST,Ig G levels. CONCLUSION The PD-1 expression on peripheral blood T cells is significantly higher in patients with AIH,which positively related to liver function indicators,and it may play an important role in the pathogenesis of AIH.
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