中华肝脏病杂志
中華肝髒病雜誌
중화간장병잡지
CHINESE JOURNAL OF HEPATOLOGY
2011年
3期
186-190
,共5页
林炳亮%谢冬英%谢俊强%张晓红%梅咏予%高志良
林炳亮%謝鼕英%謝俊彊%張曉紅%梅詠予%高誌良
림병량%사동영%사준강%장효홍%매영여%고지량
肝炎病毒,乙型%免疫,细胞%细胞因子类
肝炎病毒,乙型%免疫,細胞%細胞因子類
간염병독,을형%면역,세포%세포인자류
Hepatitis B virus%Immunity,cellular%Cytokines
目的 通过分析不同类型HBV携带者外周血单个核细胞(PBMCs)的细胞免疫功能,分析HBV抗原对其的影响,探索HBV慢性感染的机制并寻求可能的免疫治疗方法.方法 用不同的抗原和(或)细胞因子刺激培养的无症状HBV携带者PBMCs,酶联免疫吸附法检测细胞培养上清液中不同细胞因子的水平;流式细胞术检测PBMCs的细胞表型.对数据进行t检验分析和相关性分析.结果 HBsAg刺激无症状HBV携带者PBMCs后产生的干扰素(IFN)γ为(48.3±19.8)Pg/ml,较健康对照人群低[(196.2±104.3)Pg/ml(t=3.023,P＜0.05)].HBsAg和HBcAg刺激HBeAg阳性患者PBMCs分泌的IFN y水平分别为(50.4±51.6)Pg/ml和(63.2±36.9)pg/ml,明显低于HBeAg阴性组[(86.2±42.3)Pg/ml和(101.4±32.5)pg/ml],t值分别为2.468和3.184,P值均＜0.05;HBeAg阳性患者组分泌白细胞介素(IL)-12 P70明显低于HBeAg阴性组(P＜0.05);补偿外源性IL-12可明显促进HBV携带者PBMCs分泌IFN γ(P＜0.01),IL-12协同HBV抗原可激活CD8+CD45RA+CCR7及CD8+CD45RA CD62L+细胞.结论 HBeAg阳性患者PBMCs分泌IL-12减少,这可能是HBV携带者持续感染的重要原因;外源性IL-12可促进HBV携带者PBMCs中的中枢记忆性T淋巴细胞的免疫功能.
目的 通過分析不同類型HBV攜帶者外週血單箇覈細胞(PBMCs)的細胞免疫功能,分析HBV抗原對其的影響,探索HBV慢性感染的機製併尋求可能的免疫治療方法.方法 用不同的抗原和(或)細胞因子刺激培養的無癥狀HBV攜帶者PBMCs,酶聯免疫吸附法檢測細胞培養上清液中不同細胞因子的水平;流式細胞術檢測PBMCs的細胞錶型.對數據進行t檢驗分析和相關性分析.結果 HBsAg刺激無癥狀HBV攜帶者PBMCs後產生的榦擾素(IFN)γ為(48.3±19.8)Pg/ml,較健康對照人群低[(196.2±104.3)Pg/ml(t=3.023,P＜0.05)].HBsAg和HBcAg刺激HBeAg暘性患者PBMCs分泌的IFN y水平分彆為(50.4±51.6)Pg/ml和(63.2±36.9)pg/ml,明顯低于HBeAg陰性組[(86.2±42.3)Pg/ml和(101.4±32.5)pg/ml],t值分彆為2.468和3.184,P值均＜0.05;HBeAg暘性患者組分泌白細胞介素(IL)-12 P70明顯低于HBeAg陰性組(P＜0.05);補償外源性IL-12可明顯促進HBV攜帶者PBMCs分泌IFN γ(P＜0.01),IL-12協同HBV抗原可激活CD8+CD45RA+CCR7及CD8+CD45RA CD62L+細胞.結論 HBeAg暘性患者PBMCs分泌IL-12減少,這可能是HBV攜帶者持續感染的重要原因;外源性IL-12可促進HBV攜帶者PBMCs中的中樞記憶性T淋巴細胞的免疫功能.
목적 통과분석불동류형HBV휴대자외주혈단개핵세포(PBMCs)적세포면역공능,분석HBV항원대기적영향,탐색HBV만성감염적궤제병심구가능적면역치료방법.방법 용불동적항원화(혹)세포인자자격배양적무증상HBV휴대자PBMCs,매련면역흡부법검측세포배양상청액중불동세포인자적수평;류식세포술검측PBMCs적세포표형.대수거진행t검험분석화상관성분석.결과 HBsAg자격무증상HBV휴대자PBMCs후산생적간우소(IFN)γ위(48.3±19.8)Pg/ml,교건강대조인군저[(196.2±104.3)Pg/ml(t=3.023,P＜0.05)].HBsAg화HBcAg자격HBeAg양성환자PBMCs분비적IFN y수평분별위(50.4±51.6)Pg/ml화(63.2±36.9)pg/ml,명현저우HBeAg음성조[(86.2±42.3)Pg/ml화(101.4±32.5)pg/ml],t치분별위2.468화3.184,P치균＜0.05;HBeAg양성환자조분비백세포개소(IL)-12 P70명현저우HBeAg음성조(P＜0.05);보상외원성IL-12가명현촉진HBV휴대자PBMCs분비IFN γ(P＜0.01),IL-12협동HBV항원가격활CD8+CD45RA+CCR7급CD8+CD45RA CD62L+세포.결론 HBeAg양성환자PBMCs분비IL-12감소,저가능시HBV휴대자지속감염적중요원인;외원성IL-12가촉진HBV휴대자PBMCs중적중추기억성T림파세포적면역공능.
Objective To investigate the effect of HBV antigens and pathological mechanism of chronic HBV infection by analyzing the cellular immune function of peripheral blood mononuclear cells (PBMCs) from HBsAg carriers. Methods PBMCs were prepared from individuals with chronic asymptomatic HBV infection and cultured in the presence of different antigens and/or cytokines. The levels of cytokines in culture supernatants were detected by ELISA method. The phenotype of the cells was detected by FACS.Results The levels of IFN γ secreted by PBMCs from HBsAg carriers were (48.3 ± 19.8) pg/ml, significantly lower than that from healthy controls (t = 3.023, P ＜ 0.05＝; The IFN γ produced by PBMCs from HBeAg positive patients due to HBsAg and HBcAg stimulation were (50.4±51.6) pg/ml and (63.2 ± 36.9)pg/ml, significantly lower than that of HBeAg negative patients (t = 2.468 and 3.184, P ＜ 0.05, respectively＝.The IL-12p70 secreted by PBMCs from HBeAg positive patients was also significantly lower than that of HBeAg negative patients (P ＜ 0.05＝; Exogenous IL-12 promoted significantly PBMCs to secrete IFN γ (P ＜0.01＝ and IL-12 combined with HBV antigens activated CD8+CD45RA+CCR7+ and CD8+CD45RA-CD62L+cells. Conclusion IL-12 secreted by PBMCs decreased in HBeAg positive patients, which may be the crucial reason of viral persistence in chronic HBV carriers. Exogenous IL-12 combined with specific HBV antigen could promote the central memory CD8+ T cells to produce IFN γ.
