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目的:动态观测恩替卡韦治疗HBeAg阳性慢性乙型肝炎病毒携带者的临床疗效及其外周血PD-1n +CXCR5n +CD4n +T淋巴细胞、可溶性程序性死亡受体1（sPD-1）水平变化并探讨其临床意义。n 方法:慢性乙型肝炎病毒携带者治疗（A）组31例，慢性乙型肝炎患者治疗（B）组32例，慢性乙型肝炎病毒携带者未治疗（C）组15例，收集并比较3组患者0周、24周、48周外周血标本和临床资料，流式细胞技术检测PD-1n +CXCR5n +CD4n +T淋巴细胞，酶联免疫吸附法检测sPD-1水平。3组间计量资料行方差分析检验与Spearman相关性分析。n 结果:0周时，A组、C组血清HBsAg、HBeAg和HBV DNA水平均显著高于B组；外周血PD-1n +CXCR5n +CD4n +T淋巴细胞，B组（4.70%±1.58%）显著高于A组（3.25%±1.01%）和C组（2.77%±0.67%）（n F=16.65，n P0.05）；外周血sPD-1，B组［（1 866.62±1 472.70）pg/ml］显著高于A组［（824.86±538.66）pg/ml］和C组［（618.19±602.62）pg/ml］（n F=10.95，n P0.05）。48周时血清HBsAg，A组、C组较基线无显著下降（n P>0.05），均显著高于B组（n P0.05), but were significantly higher than group B (n P<0.05). Serum HBeAg levels were decreased significantly in groups A and B than baseline (n P<0.05). <0.05), but group A was significantly higher than group B (n P0.05). Serum HBV DNA level was significantly lower in groups A and B than group C (n P0.05). Peripheral blood PD-1n +CXCR5n +CD4n +T lymphocytes were significantly lower in Group A (1.56%±0.73%) and group B (1.32%±0.43%) than group C (2.64%±0.85%) (n P<0.05). Peripheral blood sPD-1 were significantly lower in group A [(289.05±215.86) pg/ml] and group B [(236.01±173.92) pg/ml] than group C [(650.34±598.46) pg/ml] (n P<0.05). There was no significant difference between group A and group B. Correlation analysis results: In group A at 48 weeks, the decreased level of PD-1n +CXCR5n +CD4n +T lymphocyte ratio had no correlation with the decreased level of HBsAg and HBV DNA, but was positively correlated with the decreased level of HBeAg (n r=0.376, n P<0.05). The decreased level of sPD-1 had no correlation with the changes of HBsAg, but was positively correlated with the decreased levels of HBeAg and HBV DNA (n r=0.598 and 0.384, n P<0.05). In group B at 48 weeks, the decreased levels of PD-1n +CXCR5n +CD4n +T lymphocytes and sPD-1 were positively correlated with the decreased levels of HBsAg, HBeAg, and HBV DNA (n P<0.05).n Conclusion:Hepatitis B virus replication and expressions in HBeAg-positive chronic hepatitis B virus carriers were significantly inhibited after 48 weeks of antiviral treatment, which is related not only to entecavir treatment, but also to the immunological mechanism involved in sPD-1. Moreover, the inhibition of HBeAg expression is associated with a decrease in the number and/or activity of PD-1n +CXCR5n +CD4n +T lymphocytes.n