摘要
目的探讨丙型肝炎感染者外周血淋巴细胞亚群与HCV基因型、肝脏炎症以及与IFN-α治疗的相互关系。方法采用流式细胞仪对41例丙型肝炎患者外周血淋巴细胞亚群百分比进行测定。同时对HCV采用限制性片段长度多态性(RFLP)进行基因分型。结果未经治疗感染者的激活T细胞(CD3+HLA-DR+)、激活CD4+T细胞(CD4+HLA-DR+、CD4+CD25+)及NK细胞(CD3-CD16/CD56+)均低于正常(P<0.05);CD8+T(CD8+CD3+)细胞、激活CD8+T细胞(CD8+HLA-DR+、CD8+CD38+)及B细胞(CD19+)均高于正常(P<0.05);在使用干扰素-α(INF-α)对有症状感染者治疗后:INF-α能显著提高受治者外周血激活T细胞(CD3+HLA-DR+)、激活CD4+T细胞(CD4+HLA-DR+、CD4+CD25+)及NK细胞(CD3-CD16/CD56+)的百分比(P<0.05);同时降低CD8+T(CD8+CD3+)细胞、激活CD8+T细胞(CD8+HLA-DR+、CD8+CD38+)及B细胞(CD19+)的百分比(P<0.05)。另外,还发现在伴有肝脏炎症的患者中,CD8+(CD8+CD3+)细胞、激活CD8+T细胞(CD8+HLA-DR+、CD8+CD38+)要明显高于不伴有炎症的者(P<0.05),而NK细胞(CD3-CD16/CD56+)则要显著低于不伴有炎症者(P<0.05);不同HCV基因型感染者外周血淋巴细胞亚群百分比差异均无统计学意义(P>0.05)。结论丙型肝炎患者细胞免疫功能存在着较严重的失调;CD8+细胞可能在丙型肝炎患者肝脏的炎症发生中起着重要作用;而INF-α的抗病毒作用的机理之一可能是通过调节机体的细胞免疫功能来实现的。不同HCV基因型感染者的细胞免疫功能未见差异。
Objective To discuss the relation of HCV genotype,INF- alpha treatment ,liver inflammation and the lym- phocyte subset of peripheral blood of HCV sufferer. Methods The lymphocyte subset of peripheral blood was assessed by flow ey- tometry and the genotype of HCV was identified by RFLP. Results After INF-alpha therapy there are a significant increase in subset of CD3 + HLA-DR + ,CD4 + HLA-DR +,CD4 + CD25 + and NK cell ( CD3-CD16/CD56 +) (P 〈 0. 05 ) and significant de- crease in subset of CD8 +CD3 +,CD8 + HLA-DR + , CD8 + CD38 +and B cell ( CD19 + ) ( P 〈 0. 05 ). The percentage of CD8+ CD3 + .CD8+ HLA-DR + and CD8 + CD38 + in case with hepatitis is higher than in case without hepatitis; but The percentage of NKcell(CD3-CD16/CD56 + ) in case with hepatitis is lower than in case without hepatitis. The genotype of HCV has nothing to do with the lymphocyte subset of peripheral blood of HCV sufferer. Coneltmlon The cellular immune function of HCV suffer is dis- order. CD8+ T cell may play important role in hepatitis C. The anti-HCV effect of INF may take effect by adjusting cellular im- mune function. There is no correlation of HCV genotype and the lymphocyte subset of peripheral blood of HCV sufferer.
出处
《四川医学》
CAS
2012年第8期1462-1465,共4页
Sichuan Medical Journal