HIV/AIDS患者CD28在外周血CD4+、CD8+ T细胞上的表达变化

目的　研究国内HIV AIDS患者CD2 8在外周血CD4 + 、CD8+ T淋巴细胞上表达的变化 ,并探讨这些变化的临床意义。方法　用流式细胞仪检测 5 1例正常对照、14例HIV感染者和 36例AIDS患者的外周血CD4 + 、CD8+ T淋巴细胞表面的CD2 8分子的表达 ,用bDNA法检测 11例HIV感染者和 18例AIDS患者的血浆病毒载量。结果　CD4 + CD2 8+ T细胞的绝对计数与百分比、CD8+ CD2 8+T细胞的百分比均显示为正常对照组 >HIV感染组 >AIDS组 ;而CD8+ CD2 8+ T细胞的绝对计数显示HIV感染组和对照组显著大于AIDS组 ,HIV感染组与对照组间差异无显著性。CD4 + 、CD2 8+ CD4 + T淋巴细胞计数与血浆病毒载量显著负相关。结论　HIV AIDS患者外周血CD2 8在CD4 + 、CD8+ T淋巴细胞上表达随着病情进展而降低 ,反映了细胞免疫功能随着疾病进展损害逐渐加重 ,是判断病情进展的指标。     

无症状期HIV感染者CD4+和CD8+T细胞计数与病毒载量的关系

艾滋病是由人类免疫缺陷病毒(human immunodeficiency virus,HIV)感染所导致的以免疫系统功能缺陷为特征的慢性高致死率传染病.CD4+T细胞是HIV损害的主要靶细胞,HIV可引起CD4+T淋巴细胞进行性丢失与功能受限[1-2].在HIV感染早期,CD8+T细胞增多并通过分泌各种细胞因子杀死被病毒感染的靶细胞,其高表达与病毒量载量呈正相关[3],而随着疾病进展,CD8+T细胞会消耗性减少.CD4+T细胞、CD8+T细胞计数与病毒载量的相关性一直为研究者关注[4-6].本研究检测了无症状期感染者,外周血CD4+T细胞和CD8+T细胞计数与病毒载量并分析它们的相关性.     

HIV-1感染疾病缓慢进展者CD8+T淋巴细胞非细胞毒性免疫应答作用的研究

目的 探讨HIV-1感染疾病缓慢进展者CD8+T淋巴细胞非细胞毒性抗病毒应答功能(CNAR)的变化.方法 应用密度梯度离心法、免疫磁珠法纯化健康人CD4+T淋巴细胞和HIV感染者CD8+T淋巴细胞,用HIV毒株SF-33感染健康人CD4+T淋巴细胞,并加入不同疾病进程HIV感染者CD8+T淋巴细胞共培养,收集培养上清,应用ELISA方法测定上清中HIV-1 p24含量.结果 我们研究发现缓慢进展组(slow progressors,SP)、HIV典型进展组(typical progressors,TP)、健康对照组及AIDS组中CNAR功能依次下降(89%>77%>73%>61%),各组间的下降差异均有统计学意义(P<0.05);在HIV感染者中,CNAR功能与CD4+T细胞绝对计数呈显著正相关;与病毒载量无显著相关性.结论 CNAR功能对HIV感染疾病不进展可能具有保护作用.     

HIV感染者外周血CD4+ CD25+ Foxp3+/CD127low/-调节性T细胞表达水平对疾病进展的影响

目的:探讨HIV感染者外周血中CD4+ CD25+Foxp3+调节性T细胞(Treg)、CD4+ CD25+ CD127low/-Treg的水平及其与其他免疫指标的关系.方法:采集68例未经抗HIV治疗的HIV/AIDS患者(长期不进展组即LTNP组29例、典型进展的HIV感染组27例、AIDS组12例)及20例健康成人的外周抗凝全血,经免疫荧光染色,应用流式细胞仪分析CD4+T细胞、CD8+T细胞、NK细胞及CD4+CD25+Foxp3+/CD127low/-Treg的含量,并进行统计学分析.结果:除CD8+T细胞外,HIV/AIDS患者外周血中CD4+T细胞、NK细胞、CD4 +/CD8+结果均明显低于健康对照组(P＜0.05);随着疾病的进展,LTNP组、HIV组、AIDS组CD4+T细胞百分比、绝对值计数,CD8+T细胞绝对计数,NK细胞绝对计数,CD4 +/CD8+比值逐渐下降,而CD8+T细胞百分比逐渐上升.对CD4+ CD25+ Foxp3+ Treg与CD4+ CD25+CD127low/-Treg百分含量、绝对计数进行多重比较发现,各组间CD4+ CD25+ Foxp3+ Treg与CD4-CD25+ CD127low/-Treg所占CD4+T细胞百分含量的差异均有统计学意义(P＜0.05),并且随着疾病的发展,CD4+ CD25+ Foxp3+/CD127low/ Treg细胞百分含量逐渐上升,LTNP组与健康对照组之间、HIV组和AIDS组之间CD4+ CD25+Foxp3+/CD127low/ Treg绝对计数差异无统计学意义(P＞0.05),其余各组间的差异均有统计学意义(P＜0.05),并且随着疾病的发展,CD4+ CD25+ Foxp3-/CD127low/-Treg绝对计数逐渐下降.结论:CD4+ CD25+ Foxp3 +/CD127low/-Treg在HIV持续感染的免疫发病机制中有一定作用.     

婴儿肠道不同部位T细胞亚群及其表面分子检测——婴儿肠道HIV-感染和复制的可能性分析

通过对婴儿外周血(PB)、肠系膜淋巴结(MLN)和肠上皮内(IE)来源淋巴细胞的比较性研究,以分析婴儿肠道HIV-1感染容许性和HIV-1复制支持性的细胞与分子基础。分离婴儿外周血单个核细胞(PBMC),肠系膜淋巴结淋巴细胞(MLNL)和肠上皮间淋巴细胞(iIEL),制备单细胞悬液,运用流式细胞术结合荧光抗体染色技术:(1)检测不同部位的CD3+T细胞中CD4+辅助性T细胞和CD8+杀伤性T细胞比例;(2)检测不同部位的CD4+T细胞CCR5和CXCR4以及CD69和HLA-DR的表达水平。结果发现:(1)iIEL中的CD4+辅助性T细胞占CD3+T细胞的比例明显低于PBMC和MLNL,而CD8+杀伤性T细胞占CD3+T细胞的比例明显高于PBMC和MLNL;(2)iIEL中CD4+T细胞CCR5和CXCR4以及CD69和HLA-DR的表达水平均明显高于PBMC和MLNL。结果表明:婴儿iIEL中CD4+T淋巴细胞与PBMC和MLNL的CD4+T淋巴细胞相比较,高表达HIV-1入胞共受体CCR5和CXCR4,提示iIEL更易被HIV-1感染;iIEL中CD4+T淋巴细胞高表达细胞活化标记分子CD69和HLA-DR,说明其更有利于HIV-1复制,这种高基础活化率可能与其不断接触小肠来源的食物和共生菌抗原有关。由此可见,婴儿肠道具有了HIV-1感染容许性和HIV-1复制支持性的细胞和分子基础,因此成了HIV-1最易感的解剖部位,这可能是围产期HIV感染的婴儿病毒载量明显高于成年人,且病情进展也比成年人快的原因。     

HIV/AIDS患者外周血T淋巴细胞亚群的研究

目的 通过对HIV/AIDS患者外周血T淋巴细胞亚群进行分析,探讨初始、记忆和效应T细胞各亚群的变化情况及其与疾病进展的关系.方法 应用流式细胞仪检测15例正常人,79例HIV/AIDS患者CD4<200组17例、200≤CD4≤500组45例和CD4>500组17例.外周血淋巴细胞中T细胞各亚群绝对数及百分比.结果随着疾病进展,CD4+ 初始细胞(Naive)计数和比例均逐渐减少(P<0.001);CD4+中枢性记忆T细胞(Tcm)计数逐渐降低(P<0.001),但百分比逐渐升高(P=0.002);CD4+效应记忆性T细胞(TEMA)百分比上升(P<0.001);CD8+Naive细胞计数及百分比均逐渐下降(P<0.05);CD8+ TCM、TEM和终末分化的效应性记忆T细胞(TEMRA)的计数及百分比,各组间差异均无统计学意义(P>0.05).结论 HIV感染者外周血T淋巴细胞亚群发生显著变化,幼稚型T淋巴细胞数目逐渐减少,功能型T淋巴细胞数目增加.本研究有助于对HIV致病机制的研究及疾病进展的监测.     

中国HIV/AIDS患者T细胞及调节性T细胞CTLA-4表达与疾病进展关系研究

目的 对中国HIV感染者T细胞及凋节性T细胞CTLA-4表达与HIV疾病进展的相关性进行研究,探讨CTLA-4在HIV感染中的作用.方法 选取58名HIV/AIDS患者(长期不进展组、无症状HIV组、AIDS组),应用流式细胞仪胞内染色技术检测T细胞及CD4+CD25+Foxp3+调节性T细胞内CTLA-4表达水平,分析其与CD4+T细胞、病毒载量、淋巴细胞活化凋亡水平的相关性.结果 长期不进展组、无症状HIV组、AIDS组CD4+T细胞内CTLA-4表达水平依次增岛(P<0.05);与CD+T细胞显著负相关(P<0.01),与CD8+T细胞活化(CD38表达)、凋亡水平(CD95表达)及CD4+T细胞凋亡水平显著相关(P<0.05),与病毒载量无显著相关性.长期不进展组、无症状HIV组、AIDS组CD8+T细胞内CTLA-4表达水平差异无统计学意义;与CD4+T细胞、病毒载量、CD4,'+>、CD8+T细胞活化及凋亡水平均无显著相关性.CD4+CD25+Foxp3+T细胞内CTLA-4表达水平长期不进展组明显低于无症状HIV组及AIDS纽(P<0.05);与CD4+T细胞显著负相关(P<0.05);与CD4+、CD8+T淋巴细胞活化(HLA-DR表达)显著相关(P<0.01).结论 中国HIV感染者CD4+T细胞及CD4+CD25+Foxp3+调节性T细胞内CTLA-4表达水平与疾病进展及免疫活化状态显著相关,参与HIV感染免疫平衡的调节.     

共抑制分子BTLA在慢性HIV-1感染中的特点及与疾病进展的相关性研究

目的:观察慢性HIV-1感染者中CD4~+和CD8~+ T淋巴细胞上BTLA(B and T lymphocyte attenuator,CD272)分子的表达及临床意义.方法:采集34例慢性HIV-1感染者和15例健康人的外周血,分离外周血单个核细胞,用间接免疫荧光染色方法标记并用流式细胞术检测T淋巴细胞上BTLA表达的百分比及平均荧光强度,并将BTLA的表达水平与患者CD4~+ T淋巴细胞计数和病毒载量做相关性分析.结果:与健康对照相比,HIV-1慢性感染者中CD4~+和CD8~+ T细胞上的BTLA表达均明显下降,且BTLA的下降在各组HIV-1慢性感染者中也有明显差异,随着疾病进展,BTLA表达进行性下降.CD4~+ T细胞上BTLA表达比率与平均荧光强度均与CD4~+T淋巴细胞计数呈明显正相关,而与病毒载量呈负相关.结论:在慢性HIV-1感染中,随着疾病进展,BTLA的进行性下降可能是机体活化和抑制信号失衡、导致免疫系统广泛活化的重要因素,恢复BTLA抑制信号的强度可能是治疗HIV感染的新策略.     

中国HIV感染长期不进展者CD4+CD25+Foxp3+调节性T细胞变化研究

目的 对中国HIV感染长期不进展者(LTNP)CD4+CD25+Foxp3+调节性T细胞水平及其与疾病进展相关性进行研究,探讨CD4+CD25+Foxp3+ 调节性T细胞在LTNP保护机制中发挥的作用.方法 选取74名HIV-1感染者(LTNP、典型进展HIV组、AIDS组)及16名健康对照,应用流式细胞仪胞内染色技术在单细胞水平检测CD4+CD25+Foxp3+调节性T细胞表达水平,分析其与CD4+ T细胞数量、病毒载量、淋巴细胞活化、凋亡水平的相关性.结果 中国HIV感染LTNP CD4+CD25+Foxp3+ T细胞百分率明显低于典型进展HIV、AIDS组及健康对照组(P<0.05).HIV/AIDS患者CD4+CD25+Foxp3+ T细胞百分率与CD4+ T细胞显著负相关(r=-0.509,P<0.001),与病毒载量明显正相关(r=0.414,P<0.01),与CD4、CD8+ T细胞表面CD38、CD95表达水平明显正相关(P<0.05),与CD4、CD8+ T细胞表面HLA-DR表达无显著相关性.结论 中国HIV感染LTNP CD4+CD25+Foxp3+ 调节性T细胞百分率明显低于典型进展者,提示调节性T细胞与LTNP保护机制相关.     

中国经采供血HIV感染长期不进展者CD4~+T淋巴细胞趋化因子受体表达研究

目的:了解中国经采供血HIV感染长期不进展者CD4+T淋巴细胞趋化因子受体表达,分析其与疾病不进展的关系。方法:收集43例经采供血HIV感染长期不进展者、82例无症状HIV感染者、35例AIDS病人及40例健康对照的抗凝全血,用流式细胞仪检测趋化因子受体CCR5、CXCR4的表达,并分析其与病毒载量、CD4+T淋巴细胞绝对值及T淋巴细胞活化的相关性。结果:长期不进展组CD4+T细胞表面CCR5的表达明显低于无症状HIV感染组及AIDS组(P0.01),与健康对照无显著差异;CD4+T细胞表面CXCR4的表达各组无显著差异。CD4+T细胞表面CCR5的表达与CD4+T细胞数量显著负相关(r=-0.498,P0.05),与病毒载量无显著相关性。CD4+T细胞表面CCR5的表达与HLA、CD38在CD4+、CD8+T细胞的表达水平显著正相关(P0.001,CD38在CD4+T细胞的表达除外),CD4+T细胞表面CXCR4的表达与HLA在CD4、CD8+T细胞的表达水平显著负相关(P0.01)。结论:HIV感染长期不进展者CD4+T细胞趋化因子受体CCR5表达维持较低水平,与疾病不进展相关。     

北京市不同转归SARS患者免疫学指标的比较性研究

目的 :探讨不同转归 (治愈 死亡 )严重急性呼吸综合征 (severeacuterespiratorysyndrome,SARS)患者病程中免疫学指标变化趋势的差异 ,以指导临床诊治和判断预后。方法 :应用SARS病历数据库 ,收集治愈和死亡SARS患者病程前 4周CD3、CD4、CD8淋巴细胞绝对值 ,CD4 CD8比值 ,淋巴细胞百分比数据 ,比较不同转归SARS患者免疫学指标的变化趋势及差异。结果 :治愈组和死亡组SARS患者CD3,CD4 ,CD8计数在起病的 1～ 2周内明显低于正常值。但治愈组各免疫学指标从第 2周起呈逐渐恢复趋势 ,而死亡组则一直呈明显降低趋势 ,第 2周仍无恢复且显著低于治愈组 (P <0 0 5 ) ,并随病程延长显著性差异更大 (P <0 0 1,P <0 0 0 1) ;CD4 CD8比值在病程中基本不变 ,无显著性组间差别。结论 :CD3、CD4、CD8淋巴细胞亚群绝对值的动态变化是判断疗效和预后的重要依据     

B cells in the aged: CD27, CD5, and CD40 expression

Ageing is characterized by numerous changes in lymphocyte subpopulations. In the present paper we have focused on B cells carrying the surface markers CD27, CD5 and CD40. CD27 is considered a marker of primed (memory) cells and its engagement promotes the differentiation of memory B cells into plasma cells. CD5 is expressed on B1 cells, which are considered to be responsible for T cell-independent antibody production other than autoantibodies. The CD40 molecule binds CD40L (CD154) and is necessary for T-dependent antibody responses. Here we show that the absolute number of CD5+ and CD40+ B cells is decreased in the elderly, while CD27+ B lymphocytes only marginally decrease in centenarians. However, there is a decrease of the percentage of CD5+ B cells, an increase of CD27+ B cells, while CD40 does not change significantly. These data, together with the increased number of NK cells during aging, suggest different regulation of antibody production in the elderly which might be another example of immune remodeling with aging, based on interactions between human B and NK cells.     

红车轴草提取物对小鼠T淋巴细胞体外活化的抑制作用

探讨红车轴草提取物(Trifolium pratense Leguminosae extract,TLE)对小鼠T淋巴细胞的体外活化的影响。无菌条件下制备小鼠淋巴细胞悬液;双色荧光抗体染色结合流式细胞术分别分析TLE对小鼠T淋巴细胞在刀豆蛋白A(ConA)或佛波醇酯(PDB)刺激下的体外分化抗原CD69、CD25、CD71表达的影响。终质量浓度为20、30、40 mg/L的TLE对小鼠T淋巴细胞在ConA或PDB刺激下的体外分化抗原CD69、CD25、CD71表达具有明显的抑制作用(P<0.01)。TLE对ConA或PDB刺激的不同时期的小鼠T淋巴细胞的体外活化具有明显的抑制作用。     

Modulation of CD4 lateral interaction with lymphocyte surface molecules induced by HIV-1 gp120

CD4, a lymphocyte surface glycoprotein, serves as co-receptor for antigen with the T cell receptor (TCR). It is also the lymphocyte receptor for HIV by binding the gp120 viral envelope protein. Interaction of gp120 with CD4 is crucial for viral infection, but is not sufficient to allow viral entry into cells. Recombinant gp120 alters CD4⁺ T cell responsiveness to activation stimuli. To express its co-receptor function fully, CD4 must be laterally associated with the TCR and CD45 to form multi-receptor complexes competent to transduce potent activation signals. Here, we examine the possibility that gp120/CD4 binding alters lateral associations of CD4 with other lymphocyte surface molecules, and that assembly of abnormal multi-molecular complexes is involved in the gp120-induced CD4⁺ T cell dysfunction and in viral entry. In the absence of gp120, CD4 displayed high association with CD3, CD5, CD45RC, CD25, CD28, CD44, and CD53; weak association with CD2, CD38, CD45RB, CD62L, and CD26; and no association with CD45RA, CD45RO, CD11b, CD11a, CD54, CD7, CD48, CD98, CD59, CD55, HLA class I and class II molecules. Treatment with gp120 significantly increased CD4 association with CD3, CD45RA, CD45RB, CD59, CD38, CD26, and HLA class I, and decreased that with CD45RC. Specificity of these results were assessed at various levels. First, gp120 did not influence lateral associations displayed by other molecules, such as HLA class II. Second, the Leu3 mAb, which binds CD4 on a site overlapping the gp120 binding site, did not elicit the same CD4 lateral associations as gp120, and finally, a direct gp120/CD4 interaction was needed to induce the lateral associations, as shown by the observation that blocking the gp120/CD4 binding by the Leu3 mAb inhibited the gp120-induced associations. These results can be interpreted in several ways. gp120/CD4 interaction could trigger an inside-out signal responsible for the associations, or gp120 could induce steric modifications of CD4 that increase its affinity for the associating molecules. Alternatively, these molecules may interact directly with gp120, bridging them with CD4. It is also possible that the associations may be mediated by additional components, interacting with both gp120 and the associating surface molecule. The last hypothesis is likely for CD59, whose gp120-induced association with CD4 required the presence of serum in the co-capping assay. Since both CD59 and gp120 bind complement, the observed association could be mediated by complement components.     

BY55/CD160 cannot be considered a cytotoxic marker in cytomegalovirus-specific human CD8(+) T cells

CD160/BY55 is a glucosyl-phosphatidylinositol (GPI)-anchored cell membrane receptor that is expressed primarily in natural killer (NK) cells. Its presence in CD8(+) T lymphocytes is considered to be a marker of cytotoxic activity, although there are few data in this regard. In the present work, we analysed the expression of CD160 in subpopulations of cytomegalovirus (CMV)-specific CD8(+) T cells. Subpopulations were defined by CD28 and CD57 expression and exhibited varying degrees of differentiation and cytotoxic potential, as evaluated by the expression of perforin, interferon (IFN)-gamma and interleukin (IL)-7Ralpha/CD127. We included subjects with different intensities of anti-viral immune response. Results showed that the terminally differentiated CD28(-) CD57(+) subset displaying the highest level of perforin expressed CD160 at a level similar to that of memory CD28(+) CD57(-)perforin(-) cells. A comparison of the expression of perforin in CD160(+) cells versus CD160(-) cells showed that expression was significantly higher in the absence of CD160. Interestingly, the CMV-specific CD8(+) T cell subset from a patient with ongoing CMV reactivation did not begin to express CD160 until day +92 of the follow-up period. Taken together, our data show that CD160 cannot be considered a cytotoxic marker in CMV-specific CD8(+) T cells.     

CD45RA and CD45RO isoforms in infected malnourished and infected well-nourished children.

The aim of this study was to determine if the distribution in vivo of CD4(+)CD45RA(+)/CD45RO(-) (naive), CD4(+)CD45RA(+)/CD45RO(+) (Ddull) and CD4(+)CD45RO(+) (memory) lymphocytes differs in malnourished infected and well-nourished infected children. The expression of CD45RA (naive) and CD45RO (memory) antigens on CD4(+) lymphocytes was analysed by flow cytometry in a prospectively followed cohort of 15 malnourished infected, 12 well-nourished infected and 10 well-nourished uninfected children. Malnourished infected children showed higher fractions of Ddull cells (11.4 +/- 0.7%) and lower fractions of memory cells (20.3 +/- 1.7%) than the well-nourished infected group (8.8 +/- 0.8 and 28.1 +/- 1.8%, respectively). Well-nourished infected children showed increased percentages of memory cells, an expected response to infection. Impairment of the transition switch to the CD45 isoforms in malnourished children may explain these findings, and may be one of the mechanisms involved in immunodeficiency in these children.     

PTA1/CD226亚家族的研究进展

免疫球蛋白超家族(IgSF)成员占细胞黏附分子(CAM)的一大部分, 通过识别细胞表面相应的配体或受体, 发挥多方面的免疫学功能.现就一组同源IgSF新成员, 包括血小板/T细胞活化抗原1(PTA1/DNAM-1/CD226)和CD96(Tactile)两个受体及其两个配体脊髓灰质炎病毒受体(PVR/CD155)和单纯疱疹病毒受体(nectin-2/CD112)的结构、相互作用、免疫学功能以及与临床的关系作一综述.     

益活清胰Ⅰ号对重症急性胰腺炎大鼠中性粒细胞与内皮细胞黏附的抑制作用

目的观察益活清胰Ⅰ号对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠的中性粒细胞(polymorphonuclear cell,PMN)-内皮细胞(endothelial cell,EC)黏附率及PMN表面黏附分子CD11/CD18表达的影响,探讨其治疗SAP的机理。方法81只SD大鼠随机分为假手术组(n=27)、造模组(n=27)、治疗组(n=27),SAP模型采用5%的牛磺胆酸钠胰胆管逆行注射方法建立。6、12、24h分批处死动物9只采集动脉血和胰腺组织标本,测定胰腺组织的MPO活性,HE染色光镜下观察胰腺组织的病理变化。分离PMN,与体外培养的血管内皮细胞作用测定PMN-EC黏附率,ELISA法测定PMN表面CD11a/CD18、CD11b/CD18。结果与假手术组比较,造模组和治疗组术后各时点胰腺组织MPO活性、PMN-EC黏附率、PMN表面CD11a/CD18和CD11b/CD18均增高(P<0.01),治疗组术后各时点胰腺组织MPO活性、PMN-EC黏附率、PMN表面CD11a/CD18和CD11b/CD18均显著低于造模组(P<0.01)。造模组胰腺组织出血和坏死严重,治疗组的病理损伤明显减轻。结论益活清胰Ⅰ号能降低PMN表面CD11a/CD18和CD11b/CD18的表达水平,减轻PMN与EC的黏附,从而有助于减轻PMN与EC黏附所致的胰腺组织病理损伤。     

隐匿型肾小球肾炎外周血CD44、CD54、CD62P的表达及意义

目的:探讨隐匿型肾小球肾炎外周血粘附分子CD44、CD54、CD62P的表达与疾病的关系。方法:采用流式细胞全血免疫荧光直标术对25例隐匿型肾小球肾炎患者外周血进行CD44、CD54、CD62P标记后,上流式细胞仪检测。结果:隐匿型肾小球肾炎患者外周血CD44、CD54、CD62P的表达显著高于正常对照(P<0.01),而且肉眼血尿组CD44、CD54、CD62P的表达显著高于尿检异常组(P<0.01)。结论:黏附分子CD44、CD54、CD62P可能介导和参与了隐匿型肾小球肾炎的发生及发展过程,外周血粘附分子CD44、CD54、CD62P的检测可为临床隐匿型肾小球肾炎的诊断和治疗提供分子依据。     

慢性乙型肝炎患者外周血淋巴细胞CD8+CD38+的检测意义

目的：通过测定慢性乙型肝炎患者外周血淋巴细胞CD8^＋CD38^＋的表达及门冬氨酸氨基转移酶（AST）、总胆红素（TBIL）、凝血酶原时间（PT），旨在为治疗慢性乙型肝炎提供有用的参考指标。方法：流式细胞术检测38例慢性乙型肝炎、14例肝硬化患者外周血淋巴细胞CD8^＋CD38^＋细胞的百分率；同时测定AST、TBIL和PT。结果：（1）慢性乙型肝炎组CD8^＋CD38^＋、CD38^＋细胞均明显高于正常组（P〈0．01，P〈0．01），肝硬化组CD8^＋CD38^＋、CD38^＋细胞均明显高于正常组（P〈0．05，P〈0．05）。肝硬化组CD8^＋CD38^＋、CD8^＋细胞均明显低于慢性乙型肝炎组（P〈0．05，P〈0．05）。（2）慢性乙型肝炎轻、中、重各组之间比较，中度组CD8^＋CD38^＋高于轻度组（P〈0．05），重度组CD8^＋CD38^＋、CD8^＋、CD38^＋均高于轻度组（P〈0．05，P〈0．05，P〈0．05）；重度组CD38^＋高于中度组（P〈0．05）；肝硬化组CD8^＋CD38‘均明显低于轻、中、重各组（P〈0．05，P〈0．01，P〈0．01），肝硬化组CD8^＋低于重度组（P〈0．01）。（3）慢性乙型肝炎患者AST、TBIL、PT不正常组CD8^＋CD38^＋均高于AST、TBIL、PT正常组。结论：慢性乙型肝炎患者CD8^＋CD38^＋细胞明显升高，表明慢性乙型肝炎患者细胞免疫处于异常激活状态，并与肝功能损伤有一定的相关性。慢性乙型肝炎患者外周血淋巴细胞CD8^＋CD38^＋的测定，对病情分析和诊断有一定的临床参考价值。