支气管哮喘患者外周血Th17、CD4~+CD25~+Treg细胞表达特征

目的:探讨外周血Th17和CD4+CD25+调节性T细胞(Treg)在支气管哮喘患者中的表达特征。方法:41例慢性持续期哮喘患者,分为间歇-轻度组(n=23)和中重度组(n=18),行肺功能检查和哮喘控制问卷(ACQ)调查,20例正常人作为对照。通过流式细胞术检测外周血Th17和CD4+CD25+Treg细胞的比例。ELISA检测血浆以及植物血凝素刺激24小时后外周血单个核细胞(PBMC)上清液中的IL-17、IL-10、TGF-β水平。结果:中重度哮喘组外周血Th17细胞比例及血浆IL-17水平高于间歇-轻度哮喘和正常人组,而外周血CD4+CD25+Foxp3+Treg细胞比例及血浆IL-10、TGF-β水平则降低。中重度哮喘组PBMC上清液中IL-17水平增高。哮喘患者FEV1(%预计值)与Th17细胞及血浆IL-17表达成负相关,与CD4+CD25+Treg表达成正相关。ACQ平均得分与Th17细胞和血浆IL-17表达成正相关,与外周血CD4+CD25+Treg表达成负相关。结论:中重度哮喘中外周血Th17细胞应答增强,而CD4+CD25+Treg细胞缺乏,哮喘的严重程度及症状控制与外周血Th17/Treg免疫应答失衡密切相关。     

Treg/Th17在变应性鼻炎患者血液中的意义

观察Treg/Th17转录因子及其细胞因子在变应性鼻炎(allergic rhinitis,AR)患者外周血单个核细胞和血清中的表达并探讨其临床意义。选择42例AR患者根据视觉模拟量表(visual analog scale,VAS)分为轻度组(n=23例)和中重度组(n=19例),同期选择20例门诊健康体检者作为对照组。采用RT-PCR检测各组Foxp3、RAR相关孤儿受体mRNA(RARrelated orphan receptor C mRNA,RORC mRNA),采用ELISA检测各组血清TGF-β和IL-17表达水平。结果显示,中重度组和轻度组变应性鼻炎患者Foxp3mRNA及血清TGF-β表达水平明显低于对照组(P<0.05),RORC mRNA和血清IL-17表达水平明显高于对照组(P<0.05),且随病情严重程度加重,Foxp3 mRNA及血清TGF-β表达水平明显降低(P<0.05),而RORC mRNA及血清TGF-β表达水平明显升高(P<0.05)。本研究证明,Treg/Th17细胞失衡可能在AR发病中占有重要的地位。     

CD4~+CD25~+调节性T细胞/Th17细胞失衡与婴幼儿脓毒症

目的 观察不同免疫状态下婴幼儿脓毒症CD4~+CD25~+Foxp3~(high)岫调节性T细胞(Tr)/Th17细胞的变化,探讨婴幼儿脓毒症适应性免疫紊乱可能的机制.方法 婴幼儿脓毒症48例,健康同龄儿童对照组26例.用流式细胞术榆测CD14~+单核细胞HLA-DR表达率,CD4~+CD25~+Foxp3~(high)Tr 比例及Th17细胞比例;用ELISA法检测细胞因子IL-1β、IL-6、IL-10、TNF-α、TGF-β及IL-17A等浓度,计算IL-10/TNF-α比值;实时荧光定量PCR(real-time PCR)检测CD4~+T细胞Foxp3、ROR-γt mRNA表达及IL-17A mRNA表达.以CD14~+单核细胞HLA-DR表达＞或＜30%为阈值,将患儿分为免疫激活组(DR-H组)和免疫抑制组(DR-L组).结果 DR-L组IL-10/TNF-α比值明显高于DR-H组(P＜0.05)及对照组(P＜0.05).CD4~+CD25~+Foxp3~(high) Tr细胞比例及转录因子Foxp3基因表达DR-L组明显高于对照组及DR-H组(P＜O.05).Th17细胞比例、IL-17A血浓度、Th17细胞IL-17A基因表达及转录因子ROR-γt基因表达DR-H组及DR-L组均明显高于对照组(P＜0.05),两组之间差异无统计学意义(P＞0.05).DR-H组和DR-L组Th17细胞主要分化调控因子IL-6、IL-1β血清浓度明显高于正常对照组(P＜0.05),两组问IL-6、IL-1β浓度差异无统计学意义(P＞0.05),DB-L组CD4~+CD25~+Foxp3~(high) Tr细胞主要调节因子TGF-β血浓度明显高于DR-H组及对照组(P＜0.05).结论 Th17持续过度活化可能是导致脓毒症前炎症细胞因子/趋化因子持续增高的原因之一;CD4~+CD25~+Foxp3~(high) Tr细胞/Th17细胞失衡可能参与脓毒症混合性拮抗反应综合征(MARS)的发生发展,婴幼儿脓毒症细胞因子微环境变化可能是导致CD4~+CD25~+Foxp3~(high) Tr细胞/Thl7细胞失衡的原因之一.     

不同类型HBV感染者外周血Treg/Th17细胞的变化及意义

目的:探讨不同类型HBV感染者外周血中CD4+ Foxp3+ Treg/Th17细胞的变化及意义.方法:选取15例急性乙型肝炎(Acute Hepatitis B,AHB)患者、40例慢性乙型肝炎(Chronic hepatitis B,CHB)患者、40例无症状携带者(Asymptomatic HBV carriers,AsC)及30例健康对照者,分别采用流式细胞术、RT-PCR和ELISA检测外周血CD4+ Foxp3+ Treg/Th17细胞百分率、核转录因子foxhead winged-helix box protein 3 (Foxp3)/retinoid-related orphan receptor gamma-t (RORγt) mRNA的表达以及血浆转化生长因子-β1(Transforming growth factor-31,TGF-β1)/IL-17的水平.结果:AHB组患者CD4+ Foxp3+ Treg/CD4+T细胞百分率、Foxp3 mRNA及TGF-β1水平与正常对照组相比无明显差异(P＞0.05);而CD4+ IL-17 +/CD4+T细胞百分率、RORγtmRNA及IL-17水平与正常对照组相比明显升高,差异有统计学意义(P＜0.05).CHB组患者CD4+ Foxp3+ Treg/CD4+T细胞百分率、Foxp3 mRNA、TGF-31水平及CD4+ IL-17 +/CD4+T细胞百分率、RORγt mRNA、IL-17水平与正常对照组相比均明显升高,差异有统计学意义(P＜0.05);与正常对照组相比,AsC组患者CD4+ Foxp3+ Treg/CD4+T细胞百分率、Foxp3 mR-NA、TGF-β1水平及CD4+ IL-17 +/CD4+T细胞百分率、RORγt mRNA、IL-17水平无明显差异(P＞0.05).结论:在不同类型HBV感染者外周血中Treg/Th17细胞失衡,Treg/Th17细胞可能与HBV感染的状态有关.     

RSV毛细支气管炎患儿血液CD4~+CD25~+Foxp3~+Treg与CD40/CD40L关系的研究

探讨CD40/CD40L信号通路对不同病原体毛细支气管炎(以下简称:毛支炎)患儿血液CD4~+CD25~+Foxp3~+ Treg的增殖分化及其分泌抑制性细胞因子TGF-β1、IL-10的影响。取呼吸道合胞病毒(RSV)及非RSV感染毛支炎患儿血液并检测CD4~+CD25~+Foxp3~+Treg的百分率;并将血液中分离的单个核细胞(PBMC)接种于24孔板内,加入CD40L McAb进行阻断,作用72h后采用流式细胞仪检测培养板内CD4~+CD25~+Foxp3~+Treg的百分率,激光共聚焦检测CD4~+CD25~+Foxp3~+Treg细胞表面Foxp3的平均密度,酶联免疫吸附法检测培养上清中TGF-β1、IL-10的含量。RSV毛支炎患儿血液中CD4~+CD25~+Foxp3~+Treg百分率显著低于非RSV毛支炎患儿及正常对照组(P<0.05);RSV毛支炎患儿体外培养PBMC中CD4~+CD25~+Foxp3~+Treg百分率均显著低于非RSV毛支炎患儿、正常对照组和抗CD40L McAb组(P<0.05)。毛支炎患儿PBMC经过体外培养72h后,抗CD40L McAb组培养的细胞中CD4~+CD25~+Foxp3~+Treg表面Foxp3的平均密度显著高于RSV毛支炎患儿组(P<0.05)。PBMC培养上清中IL-10和TGF-β1的水平抗CD40L McAb组明显高于非RSV毛支炎组,非RSV毛支炎组明显高于RSV毛支炎组,差异有统计学意义(P<0.05)。RSV毛支炎患儿体内存在严重的CD4~+CD25~+Foxp3~+Treg数量不足;体外用抗CD40L McAb阻断CD40/CD40L通路可促进RSV毛支炎PBMC中CD4~+CD25~+Foxp3~+Treg的增殖。     

CD4~+CD25~+Foxp3~+调节性T细胞在子宫内膜癌患者外周血中的表达及意义

探讨在子宫内膜癌患者外周血中CD4+CD25+Foxp3+调节性T细胞的表达情况及意义。采用流式细胞术检测84例术前子宫内膜癌患者及40例子宫肌瘤患者外周血中CD4+CD25+Foxp3+细胞比例及Foxp3平均荧光强度,采用qRT-PCR检测两组患者外周血中Foxp3的mRNA表达情况,同时采用ELISA检测外周血中TGF-β1和IL-17含量。与子宫肌瘤组比较,子宫内膜癌患者外周血中CD4+CD25+Foxp3+Treg细胞的比例虽略有升高但没有统计学意义(P=0.08),而CD4+CD25+细胞内Foxp3的平均荧光强度明显升高(P<0.001)。子宫内膜癌患者外周血中Foxp3的mRNA表达要明显多于子宫肌瘤组(P<0.001)。子宫内膜癌患者外周血中TGF-β1、IL-17的含量要多于子宫肌瘤组。子宫内膜癌患者外周血中的Foxp3+Treg细胞表达增多,这些细胞可能通过增加细胞因子TGF-β和IL-17的分泌从而调节机体对肿瘤细胞免疫反应的方向,最终促进子宫内膜癌的发生和发展。     

卡介苗多糖核酸对哮喘大鼠淋巴液和血液CD4~+CD25~+Foxp3~+调节性T细胞的影响

目的:探讨卡介苗多糖核酸(BCG-PSN)对哮喘大鼠淋巴液和血液调节性T细胞数量及功能的影响。方法:将SD大鼠随机分为对照组、哮喘组和BCG-PSN组,分别收集不同时间点大鼠淋巴液和血液,采用流式细胞仪(FCM)检测CD4+CD25+Foxp3+调节性T细胞(CD4+CD25+Foxp3+Treg)百分率,酶联免疫吸附试验(ELISA)检测淋巴液和血浆白介素10(IL-10)和转录生长因子β1(TGF-β1)浓度。结果:各组在各时间点其淋巴液中CD4+CD25+Foxp3+Treg百分率、IL-10水平均较血液明显升高。哮喘组大鼠淋巴液和血液中CD4+CD25+Foxp3+Treg百分率、IL-10、TGF-β1浓度均较对照组显著降低(P0.05)。BCG-PSN组淋巴液和血液中CD4+CD25+Foxp3+Treg百分率和IL-10水平较哮喘组明显升高(P0.05),与对照组比较无显著性差异;而TGF-β水平在48小时较对照组和哮喘组明显升高(P0.05)。结论:哮喘大鼠淋巴液和血液存在明显CD4+CD25+Foxp3+Treg数量及功能不足。BCG-PSN可能通过增加哮喘大鼠外周血和淋巴液中CD4+CD25+Foxp3+Treg的数量及其产生IL-10和TGF-β水平,增强免疫抑制效应,从而发挥抑制哮喘炎症的作用。     

1型糖尿病患儿CD4~+T细胞亚群变化初探

目的 探讨CD4~+细胞亚群[Th1、Th2、CD4~+CD25~+Foxp3~+调节性T细胞(Tr)及Th17细胞]在1型糖尿病(TIDM)患儿免疫发病机制中的作用.方法 新诊断TIDM患儿20例,同年龄对照组(Ctrl组)20例.用流式细胞术检测外周血Th1、Th2、Tr及Th17细胞比例.荧光定量PCR(real-time PCR)检测Th1、Th2、Tr、Th17细胞转录因子T-bet、GATA-3、Foxp3、ROR-γt、IFN-、IL-4、IL-10、IL-17A、CTLA-4、GITR等细胞因子和负性调节因子mRNA表达;应用酶联免疫吸附方法(ELISA)检测IFN-γ、IL-4、TGF-β、IL-6血浆水平.结果 (1)与正常对照组相比,TIDM患儿Th1细胞比例明显增高(P<0.01),Th2细胞比例明显降低(P<0.01),Tr和Th17细胞比例与正常对照组相比无明显差别(P>0.05).(2)Th1细胞转录因子及细胞因子T-bet、IFN-γ较正常对照组明显升高(P<0.01);Th2细胞转录因子及细胞因子GATA-3、IL-4明显降低(P<0.01);Tr细胞转录因子Foxp3表达与正常对照组相比差异无统计学意义(P>0.05),Tr细胞相关细胞因子及负性调节因子IL-10、CTLA-4及GITR基因表达明显低于对照组(P<0.01);Th17细胞转录因子ROR-γt及细胞因子IL-17A基因表达与对照组相比无明显差异(P>0.05);(3)TIDM患儿外周血IFN-γ浓度明显增高,IL-4明显降低,TGF-β、IL-6浓度无明显改变(P>0.05).结论 TIDM患儿Th1/Th2失衡,加上Tr细胞抑制功能缺陷,可能导致TIDM严重细胞免疫功能紊乱.     

细粒棘球蚴感染者中Tim-3~+CD4~+CD25~+Treg细胞及相关因子的表达

目的通过检测细粒棘球蚴感染者外周血中Tim-3~+CD4~+CD25~+Treg细胞及相关因子的表达水平,探讨细粒棘球蚴感染者中Tim-3与CD4+CD25+Treg细胞的关系及Tim-3+CD4+CD25+Treg细胞对该疾病持续性发展的作用。方法选取30例细粒棘球蚴感染者和30例健康对照人群,用流式细胞术检测感染组和对照组外周血中Tim-3+CD4+CD25+Treg细胞的比例变化;实时荧光定量PCR法分别检测感染组和对照组外周血单个核细胞中Tim-3和Foxp3 mRNA的表达;ELISA法检测感染组和对照组血清中IL-10和TGF-β的水平;Pearson相关法分析感染者外周血中Tim-3 mRNA的表达与Foxp3 mRNA的相关性以及Tim-3+CD4+CD25+Treg细胞与IL-10和TGF-β的相关性。结果与对照组相比,细粒棘球蚴感染组外周血中Tim-3~+CD4~+CD25+Treg细胞的比例均显著升高(P0.001);外周血单个核细胞中Tim-3和Foxp3 mRNA水平显著升高(P0.001);血清中IL-10(P0.001)和TGF-β(P=0.046)水平显著升高;细粒棘球蚴患者外周血Tim-3 mRNA与Foxp3 mRNA表达水平呈正相关;Tim-3+CD4+CD25+Treg细胞与IL-10和TGF-β的水平均正相关。结论细粒棘球蚴感染者中Tim-3在CD4+CD25+Treg细胞上的过表达可能会促进CD4+CD25+Treg细胞的产生及其抑制功能的发挥,从而促使感染的持续性发展。     

CD4~+CD25~+Foxp3~+调节性T细胞与LSCC发病的相关研究

为研究调节性T细胞在喉鳞状细胞癌(laryngeal squamous cell carcinoma,LSCC)、发展中的变化及其参与疾病进展的作用机制,收集2010～2011年上海市五官科医院收治的50例LSCC患者的肿瘤组织和外周血,应用流式细胞术检测CD4+CD25+Foxp3+Treg细胞及趋化因子受体CCR6的表达变化,Real-time PCR法检测转录因子Foxp3以及细胞因子mRNA的表达量。结果发现:LSCC患者外周血中CD4+CD25+Foxp3+Treg的百分比较正常人显著增加,并与临床分期相关;CD4+CD25+CCR6+Treg Foxp3的表达,以及肿瘤组织Foxp3mRNA的表达皆明显高于对照组,且与临床分期、淋巴结转移相关。同时发现,LSCC患者外周血中TGF-β和IL-10mRNA的检出水平分别高于对照组,但IFN-γ、IL-2、IL-12mRNA的水平低于对照组。提示此类Foxp3+Treg属于一类诱导性T抑制细胞(Foxp3+iTreg),可通过产生IL-10和TGF-β抑制LSCC患者的细胞免疫功能。Foxp3的检测可能对判断LSCC的预后有一定价值。     

CD3+ CD8+ T cell lymphocytosis masking B cell leukaemia.

A patient with CD3, CD8 positive lymphocytosis presented with features consistent with T cell chronic lymphocytic leukaemia/proliferations of large granular lymphocytes. The marrow and blood lymphoid populations (19.4 x 10(9)/l) contained more than 80% CD3 and CD8 positive cells with no evidence of a monotypic B cell population. A biopsy specimen of a vasculitic rash showed a diffuse infiltrate of CD3, CD8 positive cells into the upper dermis, consistent with T cell lymphocytic disease. After follow up for two years without treatment the blood lymphocyte count was 53 x 10(9)/l and was composed of cytologically small lymphocytes. A monoclonal SIg M D k lymphoid population (more than 90%) was demonstrable in sample blood and marrow aspirate. Gene rearrangement studies carried out on DNA extracted from peripheral blood lymphocytes at presentation and at two year follow up exhibited JH and Ck immunoglobulin gene rearrangement but no rearrangement of T cell receptor TcR gamma and beta genes. It is thought that this is the first well documented case of an aggressive CD8 positive lymphocytosis preceding, or in response to, an underlying B cell neoplasm.     

CD4+ T cell help improves CD8+ T cell memory by retained CD27 expression

CD4+ T cell help during the priming of CD8+ T lymphocytes imprints the capacity for optimal secondary expansion upon re-encounter with antigen. Helped memory CD8+ T cells rapidly expand in response to a secondary antigen exposure, even in the absence of T cell help and, are most efficient in protection against a re-infection. In contrast, helpless memory CTL can mediate effector function, but secondary expansion is reduced. How CD4+ T cells instruct CD8+ memory T cells during priming to undergo efficient secondary expansion has not been resolved in detail. Here, we show that memory CTL after infection with lymphocytic choriomeningitis virus are CD27(high) whereas memory CTL primed in the absence of CD4+ T cell have a reduced expression of CD27. Helpless memory CTL produced low amounts of IL-2 and did not efficiently expand after restimulation with peptide in vitro. Blocking experiments with monoclonal antibodies and the use of CD27(-/-) memory CTL revealed that CD27 ligation during restimulation increased autocrine IL-2 production and secondary expansion. Therefore, regulating CD27 expression on memory CTL is a novel mechanism how CD4+ T cells control CTL memory.     

CD226 对 CD4+T 细胞调节作用的研究进展

CD226 为表达于NK 细胞、T 细胞、单核细胞等多种免疫细胞膜上的一种玉型跨膜糖蛋白,与配体CD112 或CD155 结合后,通过介导多种免疫细胞的分化、增殖和功能调节来参与机体多项生理和病理活动。本文围绕CD226 对于CD4+ T 细胞的免疫调控作用和参与疾病进程的研究进展展开综述,重点阐明CD226 参与初始CD4+ T 细胞增殖分化、Th1/ Th2/Th17 细胞极化过程和对调节性T 细胞的调控作用。     

Imbalance of CD4+CD45R+ and CD4+CD29+ T helper cell subsets in patients with atopic diseases.

To evaluate the proportion of helper cell subsets we studied 18 children with atopic dermatitis, 30 patients with asthma, 27 healthy age-matched controls aged 1 to 17 years and 11 atopic controls without symptoms related to atopy, aged 9-22 years. Lymphocytes were isolated from heparinized peripheral blood and the proportion of CD4+CD29+ and CD4+CD45R+ cells was determined by double-labelling immunofluorescence. Children with atopic dermatitis yielded a significantly (P less than 0.01) higher proportion of CD4+CD45R+ (median 75%) cells compared with normal controls (median 66.6%), whereas the proportion of CD4+CD29+ cells was significantly (P less than 0.01) lower in patients with atopic dermatitis (median 20.4 versus 29.6%). Interestingly, the percentage of CD4+CD45R+ cells shows an age-dependent decline (r = -0.67, P less than 0.01) in the control group, which is not found in the patient group.     

CD4+ and CD8+ T cell responses in Helicobacter pylori-infected individuals

In order to characterize T cell responses in human Helicobacter pylori infection, we have examined proliferative responses and cytokine production by CD4+ and CD8+ T cells isolated from duodenal ulcer patients and asymptomatic H. pylori carriers, after activation with some H. pylori antigens that may be important in disease development. For control purposes, T cells from uninfected volunteers were also examined. The different H. pylori antigens induced only modest proliferative responses in circulating CD4+ and CD8+ T cells from both H. pylori-infected and uninfected individuals. However, circulating T cells from H. pylori-infected subjects produced larger amounts of interferon-gamma (IFN-gamma) in response to the Helicobacter antigens than did T cells from uninfected volunteers. Furthermore, CD8+ T cells produced larger amounts of IFN-gamma than did CD4+ T cells, on a per cell basis. Most IFN-gamma-producing cells from both infected and uninfected volunteers appeared to be naive T cells expressing CD45RA. Increased production of IL-4 and IL-5 was, on the other hand, only seen in a few instances after stimulation of isolated CD4+ and CD8+ T cells. Stimulation of freshly isolated gastric T cells with the different H. pylori antigens did not result in increased proliferation or cytokine production. In conclusion, our results show that several different purified H. pylori antigens induce production of IFN-gamma, preferentially by CD8+ cells. Therefore, they suggest that IFN-gamma-secreting CD8+ cells contribute significantly to the cytokine response induced by H. pylori infection.     

Deficiencies in CD4+ and CD8+ T cell subsets in ataxia telangiectasia

Chronic sinopulmonary infections that are associated with immunodeficiency are one of the leading causes of death in the multi-systemic disease ataxia telangiectasia (AT). Immunological investigations of AT patients revealed a broad spectrum of defects in the humoral and the cellular immune system. Based on their important role in host defence the aim of our study was an extensive analysis of cell distribution and function of CD4+ and CD8+ T lymphocytes and NK cells. We found that naive (CD45RA+) CD4+ lymphocytes, as well as CD8+/CD45RA+ lymphocytes, are decreased, whereas NK cells (CD3-/CD16+CD56+) are significantly elevated in AT patients. In our culture system proliferation and cytokine production was normal in purified memory (CD45RO+) lymphocytes after stimulation with phorbol-12,13-dibutyrate (PBu2) and after PHA activation, indicating that differences in proliferation and cytokine production are due solely to reduced numbers of CD45RA+ lymphocytes. However, activation, and especially intracellular interferon production of AT lymphocytes, seem to follow different kinetics compared to controls. In contrast to polyclonal activation, stimulation via the T cell receptor results consistently in a reduced immune response. Taken together, our results suggest that deficiency of immunocompetent cells and an intrinsic immune activation defect are responsible for the immunodeficiency in AT.     

Differential age-change in the numbers of CD4+CD45RA+ and CD4+CD29+ T cell subsets in human peripheral blood.

Peripheral blood mononuclear cells were obtained from people ranging in age from newborn to 102 years old and analyzed by dual color flow cytometer in terms of number and percentage of various subsets of T cells, B cells and natural killer cells (CD3, 4, 5, 8, 11b, 19, 20, 21, 25, 29, 45RA and 56). Numbers of T cells (CD3+ or CD5+ cells) significantly declined at the 3rd decade as compared with those of younger people, stayed at a relatively constant level between the 3rd and the 7th decade and gradually declined thereafter. In T cell subsets, both CD4 and CD8 positive positive cells decreased with age, but a decrease was more pronounced in the latter, showing an age-related increase of CD4/CD8 ratio. The most interesting finding was a contrasting age-change in two subsets of CD4+ T cells; i.e. a subset of suppressor inducer T cells (CD4+CD45RA+ naive cells) decreased with age, while a subset of helper inducer T cells (CD4+CD29+ memory cells) increased with age. CD20+ B cells also decreased with age in a manner similar to that observed in T cells. Natural killer cells (CD56) showed an increase in numbers with age. The relationship between these changes in various subsets of peripheral blood leukocytes and the age-related decline in immune functions has been discussed.     

Dynamic imaging of chemokine-dependent CD8+ T cell help for CD8+ T cell responses

Naive T lymphocytes move efficiently in lymphoid tissues while scanning dendritic cells in search of cognate complexes of peptide in major histocompatibility molecules. However, T cell migration ceases after recognition of cognate antigen. We show here that during the initiation of antigen-specific CD8(+) T cell responses, naive CD8(+) polyclonal T cells 'preferentially' interacted in an antigen-independent way with mature dendritic cells competent to present antigen to antigen-specific CD8(+) T cells. These antigen-independent interactions required expression of the chemokine receptor CCR5 on polyclonal T cells and increased the efficiency of the induction of naive, low-precursor-frequency CD8(+) T cell responses. Thus, antigen-specific CD8(+) T cells favor the priming of naive CD8(+) T cells by promoting the CCR5-dependent recruitment of polyclonal CD8(+) T cells to mature dendritic cells.     

小细胞和非小细胞肺癌晚期患者CD3~+ CD4~+及CD3~+ CD8~+T淋巴细胞亚群的差异

目的:探索小细胞和非小细胞肺癌晚期患者CD3+CD4+及CD3+CD8+T淋巴细胞亚群是否存在差异,并为治疗提供参考。方法:选取肺癌晚期患者共65例,其中包括小细胞肺癌14例,非小细胞肺癌51例以及20例健康对照。用流式细胞仪检测研究对象外周血淋巴细胞表面CD3+CD4+及CD3+CD8+的表达情况。结果:CD3+CD4+T细胞所占比例无论是小细胞还是非小细胞肺癌晚期的患者都较健康对照显著降低;CD3+CD8+T细胞所占比例在肺癌晚期的患者较健康对照并无显著变化;CD4+/CD8+比值在小细胞肺癌晚期患者较健康对照显著下降。结论:无论是小细胞还是非小细胞肺癌晚期的患者CD3+CD4+T细胞的水平较健康人都显著降低,说明肺癌晚期患者细胞免疫功能严重受损。     

CD3+CD4-CD8- alphabeta-TCR+ T cell as immune regulatory cell

Down-regulation of immune responses by regulatory T cells is one of the major mechanisms involved in the induction of tolerance to self- and alloantigens as demonstrated in a number of models of transplantation and autoimmunity. It is clear that regulatory T cells consist of different subsets. Recently a novel subset of antigen-specific alphabeta-TCR+ CD4-CD8- (double negative, DN) regulatory T cells has been found to be able to inhibit the function of the CD8+ T cells carrying the same T cell receptor specificity and prevent the rejection of skin allografts. Identification of the DN regulatory T cells and their novel mechanism of suppression can help us to understand how donor-specific transplantation tolerance can be achieved and to explain how tolerance to self-antigens can be maintained in the periphery.