自身免疫性肝炎患者外周血T细胞PD-1的表达及与肝功能指标的相关性

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 IgG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。

Expression of PD-1 on Peripheral Blood T Cells and the Correlation with Liver Function Indicators in Patients with Autoimmune Hepatitis

ABSTRACT:OBJECTIVE To investigate the percentage of programmed cell death receptor 1 ( PD-1 ) on periph-eral blood CD4 +,CD8 +T cells and explore the correlation with liver liver function indicators in patients with autoim-mune 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,IgG levels.CONCLUSION The PD-1 expression on peripheral blood T cells is significantly high-er in patients with AIH,which positively related to liver function indicators,and it may play an important role in the pathogenesis of AIH.