无症状期艾滋病HIV感染者CD+4 CD+8 T淋巴细胞检测结果分析

目的分析本地区人类免疫缺陷病毒(HIV)感染者免疫力被破坏情况,制订相应的艾滋病(AIDS)防治方案.方法对1344例无症状HIV感染者进行CD+4、CD+8 T淋巴细胞检测.结果发现18例免疫力极度低下(CD+4＜30个/mm3)的处于无症状期的HIV感染者,其CD+8T淋巴细胞值≥(400～800个/mm3).结论无症状的HIV感染者中存在着免疫力极度低下者,由于高水平的CD+8T淋巴细胞的抗病毒作用而使之处于无症状期,但其免疫系统已严重受损,任何机会性感染都会诱发他们发展为AIDS.测定其CD+4、CD+8T淋细胞作为预见HIV感染状态和进展为AIDS的重要参考指标,具有不可替代的作用.     

CD8~+ T淋巴细胞对HIV感染者生存质量的作用

目的分析探讨CD8+ T淋巴细胞对HIV感染者生存质量的作用,为提高患者的生存质量和免疫重建提供思路。方法对844例感染HIV病毒14年以上的艾滋病感染者和艾滋病患者,进行CD4+和CD8+ T淋巴细胞检测。结果发现25例长期感染者,CD4+ T细胞低下≤200个/mm3个,但CD8+ T细胞≥800个/mm3,他们没有并发症状,身体基本健康,生存质量明显高于有并发症的艾滋病患者。结论高水平的CD8+ T淋巴细胞,对于感染者抵抗并发症状,提高生存质量可能起到非常重要的作用,提示CD8+ T淋巴细胞在患者免疫重建和对抗击HIV病毒可能起到了重要的作用。     

罗定市2014年新发现HIV感染者首次CD4+T淋巴细胞检测情况分析

目的 了解人类免疫缺陷病毒(HIV)新感染者的首次CD4+T淋巴细胞检测情况,尽早发现机体免疫功能情况,为艾滋病防治工作提供有力的科学依据。方法 对罗定市2014年新发现的HIV感染者采取全血样本,用流式细胞仪进行CD4+T淋巴细胞检测并统计分析检测数据。结果 共检测83例HIV/艾滋病(AIDS)的外周血样本,HIV/AIDS首次检测的CD4+T淋巴细胞均值为(158.04±180.45)个/μl,其中≤200个/μl有54例,占65.06%;201~350个/μl有22例,占26.51%;351~500个/μl有2例,占2.41%;CD4>500个/μl有5例,占6.02%。不同性别CD4+T淋巴细胞计数比较,差异无统计学意义(t=-1.569,P>0.05)、不同年龄CD4+T淋巴细胞计数比较,差异有统计学意义(F=6.480,P<0.05)。结论 HIV感染者首次CD4+T淋巴细胞免疫水平较低,HIV感染者发现较晚。早发现、早治疗是防治AIDS的重要措施。对新发现的HIV感染者进行首次CD4+T淋巴细胞检测,以便及时发现是否感染或是否需要及时进行抗病毒治疗,以提高机体免疫力,从而降低机会性感染和病死率,提高患者生存质量。     

HIV/HCV共感染者T淋巴细胞亚群CD_(28)、CD_(38)分子表达特征的分析

目的通过观察HIV/HCV共感染者外周血T淋巴细胞亚群CD_(28)、CD_(38)分子的表达规律,探讨其与疾病进展的相关性。方法本研究选择本院2012年8月至2014年10月门诊HIV感染者40例、HIV/HCV共感染患者40例及体检中心2014年9~10月体检健康人群20例,采用流式细胞术检测HIV/HCV共感染患者(40例)、HIV感染者(40例)和健康人(20例)外周血CD_8~+T淋巴细胞表面CD_(28)、CD_(38)分子的表达,分析HIV/HCV共感染者CD_(28)、CD_(38)分子在T淋巴细胞亚群的表达特征;按照CD4~+T数值对HIV/HCV共感染者进行分组,分析不同CD4~+T水平CD_8~+CD_(28)~+、CD_8~+CD_(38)~+的表达差异,探讨CD_8~+T淋巴细胞CD_(28)、CD_(38)分子与疾病进展的相关性。结果与健康人群及HIV感染者比较,HIV/HCV共感染者CD_8~+CD_(38)~+T细胞的绝对计数与百分比明显升高,CD_8~+CD_(28)~+T细胞百分比明显降低;随着CD4~+T水平的降低,CD_8~+CD_(28)~+T有逐渐降低趋势,CD_8~+CD_(38)~+T有逐渐升高趋势。结论 HIV/HCV共感染者CD_8~+T淋巴细胞表面CD_(28)分子表达降低,CD_(38)分子表达升高,且这种变化与患者CD4~+T水平密切相关,可作为判断疾病进展的重要指标。     

851例HIV/AIDS患者抗病毒治疗后病毒载量和CD4+T淋巴细胞检测结果分析

目的 了解郑州市851例HIV/AIDS患者抗病毒治疗后免疫重建效果及病毒抑制情况,分析病毒载量与CD4+T淋巴细胞的相关性.方法 采集HIV/AIDS患者的外周血用于CD4+T淋巴细胞的计数,分离血浆后采用荧光探针法检测病毒载量(VL).应用SPSS 22.0对数据进行统计分析.结果 抗病毒治疗后,58.99％患者C...     

猪囊尾蚴病患者CD4~+ CD25~+调节性T细胞水平的变化

目的检测猪囊尾蚴病患者外周血中CD4+CD25+调节性T淋巴细胞及其FOXP3的表达情况,探讨CD4+CD25+调节性T淋巴细胞在猪囊尾蚴感染中的免疫调控作用及意义。方法采用流式细胞仪检测11例猪囊尾蚴病患者外周血中CD4+CD25+T淋巴细胞的含量,同时观察CD4+CD25+T细胞中表达FOXP3群体的百分含量。结果囊尾蚴病患者外周血中CD4+CD25+T淋巴细胞的百分含量为6.11%,较正常人(3.94%)明显升高(P<0.05);患者外周血中CD4+CD25+T细胞表达FOXP3的细胞百分含量为15.67%,与正常对照组(11.09%)有显著性差异(P<0.05)。结论猪囊尾蚴病患者外周血中CD4+CD25+T淋巴细胞的百分含量显著升高,表明CD4+CD25+调节性T细胞可能参与猪囊尾蚴感染的免疫抑制。     

T-SPOT联合CD4~+T淋巴细胞计数早期诊断HIV/AIDS合并肺结核潜伏感染的诊断价值分析

目的探讨结核(TB)感染T细胞酶联免疫斑点试验(T-SPOT)与CD4~+T淋巴细胞计数联合应用对艾滋病(HIV/AIDS)合并肺结核潜伏感染(LTBI)早期诊断的价值。方法选取2014年7月~2017年4月我院人类免疫缺陷病毒(HIV)阳性(+)感染者20例,其中合并LTBI的10例患者作为HIV(+)TB待排组,其余作为单纯HIV(+)组;HIV阴性(-)30例,合并LTBI的10例患者作为HIV(-)TB待排组,其余作为单纯HIV(-)组。以诊断TB标准(病原学检验)做参照,以上述四组人员为对象,比较结核菌素实验(TST)和T-SPOT诊断TB的灵敏度、特异性、准确度、阳性预测值和阴性预测值,比较TST与T-SPOT诊断TB的一致性,以及CD4+细胞计数对两者的影响。结果 T-SPOT在TB诊断中,灵敏度、特异度、准确度均明显高于TST,在HIV(+)TB待排组和HIV(-)TB待排组中,T-SPOT和TST诊断TB一致性良好(Kappa>0.75)。CD4~+T淋巴细胞计数增加能够引起T-SPOT与TST对TB诊断的灵敏度、特异性和准确性的明显增加,且T-SPOT优于TST。结论在AIDS合并LTBI人群中,T-SPOT对TB诊断的灵敏度、特异性和准确度均明显高于TST,且T-SPOT对TB的诊断价值随着CD4~+T淋巴细胞计数增加而提高。     

CD4+CD25+调节性T细胞在再生障碍性贫血中的表达及意义

目的:探讨再生障碍性贫血(再障)患者治疗前、后外周血T淋巴细胞亚群、CD4+CD25+T细胞的变化及其临床意义.方法:采用流式细胞术检测23例再障患者治疗前、后外周血T淋巴细胞亚群、CD4+CD25+T细胞的比例,并与健康对照组进行比较.结果:(1)再障患者治疗前CD4+,CD4+/CD8+,CD4+CD25+明显低于健康对照组(P＜0.01),CD8+细胞则明显升高(P＜0.05);重型再障组与慢性再障组比较CD4+CD25+降低,但差异不显著(P＞0.05),CD3+,CD4+,CD4+/CD8+,CD4+CD25+无统计学意义.(2)再障患者治疗后与治疗前相比,CD4+,CD4+/CD8+,CD4+CD25+明显升高(P＜0.01).(3)再障患者治疗有效者与无效者比较CD4+,CD4+/CDs+,CD4+CD25+明显升高(P＜0.01).结论:再障患者存在T淋巴细胞亚群的失调及CD4+CD25+T淋巴细胞的异常表达,且检测外周血T淋巴细胞亚群、CD4+CD25+T细胞有助于了解再障患者的免疫状态、疗效评价及预后判断.     

支原体肺炎儿童外周血CD4+CD25+调节性T细胞水平的变化及维生素A的调节作用

目的 探讨肺炎支原体肺炎(MPP)患儿外周血淋巴细胞中CD4+ CD25+调节性T细胞(Treg)、T细胞亚群CD3+、CD4+、CD4+/CDs水平的变化及临床意义;探讨体外实验时维生素A体内活性代谢产物视黄酸对MPP患儿外周血淋巴细胞CD4+ CD25+ Treg细胞、T细胞亚群CD3+、CD4+表达及CD4+/CD8+比率的调节干预作用.方法 选择2012年10-12月在空军总医院儿科确诊为MPP的20例住院患儿作为研究对象,其中10例患儿作为病例试验组,另10例患儿作为病例对照组(即未与视黄酸孵育),同期10例同龄健康儿童作为正常对照组.收集患儿及正常对照儿童外周血标本,分离单个核细胞,用流式细胞仪检测外周血淋巴细胞中CD4+ CD25+ Treg细胞、T细胞亚群CD3+、CD4+、CD4+/CD8+水平,病例试验组提取其淋巴细胞在体外培养基中加入一定量视黄酸共同培养孵育,再次测定CD4+ CD25+ Treg细胞、T细胞亚群CD3+、CD4+、CD4+/CD8+水平,将上述指标进行比较分析.结果 病例组患儿外周血淋巴细胞中CD4+ CD25+ Treg细胞、CD4+/CD8+、CD3+百分比分别为(4.5±1.9)％、(1.3±0.9)％、(38.9±11.4)％,正常对照组儿童分别为(13.2±2.5)％、(7.9±3.0)％、(65.1±8.8)％,病例对照组明显低于正常对照组,差异有统计学意义(P＜0.05),而与视黄酸共同孵育后病例试验组以上指标明显升高,分别上升至(9.2±3.8)％、(5.9±2.5)％、(81.3±11.6)％,与病例对照组比较差异有统计学意义(P＜0.05),与正常对照组比较差异无统计学意义(P＞0.05).结论 MPP患儿外周血淋巴细胞中CD4+ CD25+ Treg细胞、CD3+T细胞表达明显受抑,CD4+/CD8+亚群比例异常,T细胞亚群数量及功能明显紊乱,而体外试验时维生素A体内活性代谢产物视黄酸干预后能增强淋巴细胞CD4+ CD25+ Treg细胞、CD3+ T细胞表达,恢复CD4+/CD8+亚群比例,纠正T细胞亚群功能失衡,从而增强、协调机体免疫、抗感染能力,为维生素A辅助治疗MPP提高参考.     

105例HIV+/AIDS患者T淋巴亚群检测结果分析

目的探讨HIV+/AIDS患者T淋巴细胞亚群的改变。方法对105例HIV+/AIDS患者进行CD3、CD4、CD8、CD4/CD8比值测定,分为HIV+组和AIDS组,并与正常人对照组比较。结果 CD3各组变化不明显;CD4:HIV+组及AIDS组明显低于正常人(P<0.05),CD8:HIV+组及AIDS组高于正常人对照组,HIV+高于AIDS组;CD4/CD8比值:HIV+及AIDS组低于正常对照组。结论 HIV感染后CD4、CD4/CD8比值降低,CD8代偿增高,至AIDS期CD8失代偿后逐渐降低,HIV+患者应对T淋巴细胞亚群多个指标进行检测。     

CD4+CD25+调节性T细胞与儿科疾病

古希腊特尔斐阿波罗神庙上镌刻着一句铭言:Gnothi Seauton(英文为know thyself)即"认识自己"."认识自己"已成为免疫学家广为认可的定律:机体免疫系统首先必须识别自身的抗原,产生无反应性,再针对外来抗原产生免疫应答,即"识别自身,排斥异己".     

孕妇外周血CD4+CD25+调节性T细胞对子痫前期的预测

目的:探讨孕妇外周血CD4+ CD225+调节性T细胞(CD4 CD25+ Tregs)对子痫前期的预测价值.方法:选取190例于我院产前常规孕期体检及分娩的孕产妇作为研究对象,按孕产妇是否发生子痫前期分为子痫前期组及正常对照组,采用流式细胞仪测定各孕妇20～24周外周血单个核细胞(PBMC)中CD4T细胞及CD4 CD25+ Tregs的比率,并随访至分娩.采用磁珠分选技术分选随访期间确诊子痫前期的患者外周血PBMC中CD4 CD25+ Tregs和CD4CD25T细胞,酶联免疫仪检测CD4 CD25+ Tregs对CD4CD25T细胞增殖的抑制作用,并与正常孕妇组对比.结果:①随访情况.190例孕产妇妊娠期内有15例发展为子痫前期,其余175例为正常分娩,2组在剖宫产率、胎儿心率异常率、新生儿1 min及5 min的Apgar评分有显著性差异(P＜0.05).②CD4 CD25+ Tregs的数量.子痫前期组和正常对照组外周血PBMC中CD4T细胞比率分别为34.21％±6.92％和35.72％±7.45％,2组比较无显著性差异(P＞0.05).子痫前期组外周血PBMC中CD4 CD25+ Tregs占CD4T细胞的比率为6.71％±2.21％,明显低于正常对照组的12.01％±2.98％(P＜0.05).③CD4 CD25+ Tregs的抑制功能.子痫前期组CD4 CD25+ Tregs对CD4 CD25-T细胞增殖的抑制百分率为57.56％±9.47％,正常孕妇组为78.27％±12.43％,2组比较有显著性差异(P＜0.05).④CD4 CD25+ Tregs的预测性.以CD4+ CD25+ Trges数量变化预测子痫前期的ROC曲线下面积为0.913,Tregs的最佳截断点为6.605％,预测子痫前期的敏感度86.7％、特异度82.85％.结论:孕妇妊娠中期外周血CD4 CD25+ Tregs数量减少和(或)抑制功能下降与子痫前期的发生相关,可作为子痫前期的预测性指标.     

The generation and antigen-specificity of CD4+CD25+ regulatory T cells

CD4+CD25+ regulatory T cells are essential components of the immune system. They help to maintain immune tolerance by exerting suppressive effects on cells of the adaptive and innate immune system. In the last few years there has been an abundance of papers addressing the suppressive effects of CD4+CD25+ regulatory T cells and their putative role in various experimental disease models and human diseases. Despite the enormous amounts of data on these cells a number of controversial issues still exists. CD4+CD25+ regulatory T cells were originally described as thymus-derived anergic/suppressive T cells. Recent papers however indicate that these cells might also be generated in the periphery. Due to the thymic development of CD4+CD25+ regulatory T cells it was thought that these cells were specific for self-antigens. Indeed it was shown that CD4+CD25+ regulatory T cells could be positively selected upon high affinity interaction with self-antigens. However, evidence is accumulating that these cells might also interact with non-self antigens. Finally, in the literature there is conflicting evidence regarding the role of soluble factors versus cell-contact in the mechanism of suppression. The aim of this review is to summarize the evidence supporting these opposing viewpoints and to combine them into a general model for the origin, function and antigen-specificity of CD4+CD25+ regulatory T cells.     

CD4+CD25+ regulatory T cells in health and disease

1. Over the past 5 years, tremendous progress has been made in understanding the suppressive mechanisms of T regulatory (Treg) cells. The Treg cells, a subpopulation of T cells, have been shown to play an important role in maintaining peripheral tolerance and the prevention of autoimmunity. 2. Various populations of Treg cells have been described, including thymically derived CD4(+)CD25(+) Treg cells. These naturally occurring Treg cells are present in the periphery and are capable of suppressing proliferation and effector T cell responses both in vitro and in vivo. 3. In addition, a second subset of Treg cells, type 1 T regulatoary (Tr1) and Th3 cells, exert their suppressive capacity via cytokines such as interleukin-10 and transforming growth factor-beta and are contact independent. 4. The present review summarizes the characteristics and molecular basis of CD4(+)CD25(+) Treg cells, as well as their therapeutic potential in modulating inflammatory diseases, such as inflammatory bowel disease and rheumatoid arthritis.     

Targeting CD4+CD25+FoxP3+ regulatory T-cells for the augmentation of cancer immunotherapy

CD4+CD25+FoxP3+ T-regulatory (Treg) cells are vital to the maintenance of peripheral self tolerance and are implicated in tolerance to foreign antigens. Increasing evidence shows that Treg cells may also play an important role in immune evasion mechanisms employed by cancer. Treg cells are actively recruited and induced by tumors to block innate and adaptive immune priming, effector function and memory response, which can inhibit the efficacy of therapeutic cancer vaccines. As such, modulation of Treg cell function in cancer has been studied using various approaches, with encouraging preclinical and clinical findings. However, controlled and effective modulation of Treg cell function for cancer therapeutics will be contingent on a better understanding of the molecular basis of Treg cell interaction with tumor cells and ensuing immunosuppressive mechanisms.     

Generation of CD2+CD8+ NK Cells from c-kit+ Bone Marrow Cells in Porcine

Natural killer (NK) cells provide one of the initial barriers of cellular host defense against pathogens, in particular intracellular pathogens. Because bone marrow-derived hematopoietic stem cells (HSCs), lymphoid protenitors, can give rise to NK cells, NK ontogeny has been considered to be exclusively lymphoid. Here, we show that porcine c-kit⁺ bone marrow cells (c-kit⁺ BM cells) develop into NK cells in vitro in the presence of various cytokines [interleukin (IL)-2, IL-7, IL-15, IL-21, stem cell factor (SCF), and fms-like tyrosine kinase-3 ligand (FLT3L)]. Adding hydrocortisone (HDC) and stromal cells greatly increases the frequency of c-kit⁺ BM cells that give rise to CD2⁺CD8⁺ NK cells. Also, intracellular levels of perforin, granzyme B, and NKG2D were determined by RT-PCR and western blotting analysis. It was found that of perforin, granzyme B, and NKG2D levels significantly were increased in cytokine-stimulated c-kit⁺ BM cells than those of controls. And, we compared the ability of the cytotoxicity of CD2⁺CD8⁺ NK cells differentiated by cytokines from c-kit⁺ BM cells against K562 target cells for 28 days. Cytokines-induced NK cells as effector cells were incubated with K562 cells as target in a ratio of 100:1 for 4 h once a week. In results, CD2⁺CD8⁺ NK cells induced by cytokines and stromal cells showed a significantly increased cytotoxicity 21 days later. Whereas, our results indicated that c-kit⁺ BM cells not pretreated with cytokines have lower levels of cytotoxicity. Taken together, this study suggests that cytokines-induced NK cells from porcine c-kit⁺ BM cells may be used as adoptive transfer therapy if the known obstacles to xenografting (e.g. immune and non-immune problems) were overcome in the future.     

雷帕霉素诱导大鼠体内CD4+CD25+FoxP3+调节性T细胞的增殖

目的 探讨雷帕霉素(RPM)对大鼠CD4+CD25+FoxP3调节性T细胞的影响.方法 大鼠20只随机均分为两组:实验组RPM 2 mg·kg-1·d-1灌胃2周;对照组用生理盐水替代.无菌件下下腔静脉采血,并分离脾脏及胸腺,制备单个核细胞悬液.采用流式细胞术检测大鼠外周血、脾脏及胸腺内CD4+CD25+T细胞的占单个核细胞的比例,实时定量-PCR检测脾脏细胞FoxP3 mRNA表达,ELISA检测外周血血清转化生长因子β(TGF-13)和白细胞介素10(IL-10)含量.结果 实验组外周血、脾脏和胸腺中CD4+CD25+T细胞的比例明显高于对照组(P＜0.05).实验组大鼠脾脏细胞FoxP3 mRNA表达为对照组的4.1倍.实验组TGF-β和IL-10显著高于对照组(P＜0.05).结论 RPM能诱导大鼠体内CD4+CD25+FoxP3+调节性T细胞增殖,且增加体内免疫抑制性细胞因子TGF-β和IL-10的分泌.     

Resveratrol induces the suppression of tumor-derived CD4+CD25+ regulatory T cells

CD4+CD25+ regulatory T cells (Treg cells) are negative regulator of the immune system and main obstacles to cancer immunotherapy in tumor-bearing hosts. Resveratrol is a natural product found in grapes with both immunomodulatory and anticancer effects, which can be controlled by Treg cells. Therefore, to determine whether resveratrol performs these actions via Treg cells, we investigated changes in Treg cell population and immunomodulatory cytokines in EG7 tumor-bearing C57BL/6 mice. In the present study, CD4+CD25+ cell population among CD4+ cells was inhibited ex vivo by resveratrol treatment in a dose-dependent manner. FoxP3+ expressing cells among CD4+CD25+ population were significantly reduced after resveratrol treatment ex vivo in intracellular FACS analysis. Single intraperitoneal administration of 4 mg/kg resveratrol suppressed the CD4+CD25+ cell population among CD4+ cells and downregulated secretion of TGF-beta, an immunosuppressive cytokine, measured from the spleens of tumor-bearing mice. Furthermore, resveratrol enhanced IFN-gamma expression in CD8+ T cells both ex vivo and in vivo,leading to immune stimulation. Taken together, these results suggest that resveratrol has a suppressive role on CD4+CD25+ cell population and makes peritumoral microenvironment unfavorable to tumor in tumor-bearing mice. Thus, resveratrol can be considered as possible adjuvant material for vaccination-based cancer therapy.     

CD8+CD103+ regulatory T cells in spontaneous tolerance of liver allografts

It has been shown that rat liver allografts between certain inbred major histocompatibility complex (MHC) disparate strains are accepted spontaneously, and regulatory T cells (Tregs) have been suggested to play a role in the spontaneous liver tolerance. CD8⁺CD103⁺ T cells bear the phenotypes of effector cells, and they are implicated in allograft destruction. Here we provide evidence that CD8⁺CD103⁺ T cells possess regulatory function and may contribute to prevent liver allograft rejection. We show that the expression of CD103 in the CD8⁺ T cells was increased in spontaneous liver grafts tolerant recipients. We further show that CD8⁺CD103⁻ T cells can also upregulate the expression of CD103 and Foxp3 after stimulation with alloantigen or TGF-β in vitro, and the CD8⁺CD103⁺ T cells acquired regulatory properties. The suppressive function of the alloantigen or TGF-β conditioned CD8⁺CD103⁺ T cells was cell–cell contact dependent. These results imply that liver-specific factor(s) would be involved in the generation of CD8⁺CD103⁺ Tregs that contribute to spontaneous liver allografts tolerance.