CXCR5~+CD8~+ T细胞在HIV感染中的免疫特征及其与疾病进展关系的研究

目的探讨HIV感染者外周血CXCR5~+CD8~+T细胞的频率、功能变化及其与病情进展的相关性。方法收集40例HIV感染者和15例健康对照者,采用流式细胞分析术检测其外周血CXCR5~+CD8~+T细胞频率及IFN-γ和IL-10表达,并分析其与血浆HIV载量和外周血CD4~+T细胞计数的相关性。结果与健康对照组相比,HIV感染组外周血CXCR5~+CD8~+T细胞频率上调(P0.05),且与外周血CD4~+T细胞计数呈弱正相关(r=0.349,P=0.027),与血浆HIV载量呈弱负相关(r=-0.377,P=0.040);HIV感染者外周血CXCR5~+CD8~+T细胞IFN-γ表达与血浆HIV载量呈负相关(r=-0.514,P=0.002);而CXCR5~+CD8~+T细胞IL-10的表达在HIV感染者中明显上调(P0.05),与外周血CD4~+T细胞计数呈弱负相关(r=-0.317,P=0.046),与血浆HIV载量呈正相关(r=0.670,P=0.002)。结论 HIV感染者外周血CXCR5~+CD8~+T细胞频率功能变化与疾病进展密切相关。     

慢性丙型肝炎患者CD4+CD25+调节性T细胞表达增加

目的:探讨CD4+CD25+调节性T(Treg)细胞在慢性丙型肝炎患者免疫下调中的意义.方法:流式细胞仪检测慢性丙型肝炎患者外周血中CD4+CD25+Treg细胞的数量;与CD4+CD25-T细胞共同培养,检测其抑制功能;流式细胞仪检测其对CD4+CD25-T细胞合成IFN-γ和IL-4的影响;RT-PCR检测CD4+CD25+Treg细胞中Foxp3的mRNA表达.结果:CD4+CD25+Treg细胞约占慢性丙型肝炎患者外周血中CD4+T细胞的14.1±1.6%,显著高于正常对照5.3±0.8%(P＜0.01),显著抑制CD4+T细胞的增殖(P=0.002),以及合成IFN-γ.CD4+CD25+Treg 细胞高表达Foxp3.结论:持续性HCV感染患者CD4+CD25+Treg细胞表达增加,特异性抑制Th1细胞反应.     

慢性乙型肝炎患者外周血调节性T细胞及其相关细胞因子水平检测及临床意义

目的探讨慢性乙型肝炎病毒感染者外周血CD4+CD25+调节性T细胞(Treg)、IL-18、IFN-γ、TGF-β水平变化及临床意义。方法选择乙型肝炎病毒携带者(ASC)112例、慢性乙型肝炎患者(CHB)63例和健康对照者50例,采用流式细胞术和ELISA法分别检测CD4+CD25+细胞和IL-18、IFN-γ、TGF-β水平;采用荧光定量聚合酶链反应法检测HBV DNA载量。结果CHB患者外周血CD4+CD25+Treg细胞数、IL-18、IFN-γ、TGF-β水平分别为(30.97±18.78)%、(448.51±75.75)ng/ml、(190.93±38.52)ng/ml和(331.22±71.67)ng/ml,ASC组分别为(28.17±18.52)%、(524.52±81.42)ng/ml、(204.93±47.77)ng/ml和(336.01±82.61)ng/ml,均显著高于健康人[分别为(27.30±17.59)%、(49.79±25.68)ng/ml、(14.41±11.75)ng/ml和(42.28±17.50)ng/ml,P0.05]。结论乙型肝炎病毒感染者存在CD4+CD25+Treg细胞数的变化,IL-18、IFN-γ和TGF-β可能参与了乙型肝炎患者肝损伤过程。     

辅助性T细胞在支气管哮喘患者的表达及其意义探讨

目的探讨CD+4CD+29辅助性T细胞在支气管哮喘发病机制的作用。方法选取非急性发作期支气管哮喘患者及肺炎患者各30例,以及30例健康志愿者作为对照,使用流式细胞术检测外周血CD+4CD+29辅助性T细胞及其胞内细胞因子γ干扰素(IFN-γ)及白介素4(IL-4)的频率。哮喘患者使用氨茶碱片进行治疗,4周后复测CD+4CD+29T细胞及其细胞因子。结果哮喘患者患者CD+4CD+29T细胞及IL-4均明显高于肺炎组及健康志愿者组(P0.05),但后两者无组间统计学差异;哮喘组与肺炎组IFN-γ无组间显著性差异,但均显著低于对照组(P0.05)。治疗后哮喘组患者CD+4CD+29T细胞含量明显降低,IFN-γ明显回升,IL-4明显下降(均为P0.05)。结论 CD+4CD+29辅助性T细胞含量升高是哮喘的一个免疫机制,该细胞分泌的IL-4诱发Th2类免疫反应,可介导哮喘的体液免疫从而加重病情。     

结核性胸膜炎患者胸液中CD4~+ CD25~+ FoxP3~+调节T细胞抑制抗结核免疫

目的研究结核性胸膜炎患者胸液中CD4+CD25+FoxP3+调节T细胞是否增多,这些调节T细胞是否抑制结核的特异细胞免疫反应。方法使用细胞分离、流式细胞分析及体外细胞培养作细胞增殖及增殖抑制等实验方法,对15例结核性胸膜炎患者及17例健康正常人群胸液及外周血白细胞中CD4+CD25+FoxP3+调节T细胞的量及特征作研究。结果结核性胸膜炎患者胸液中CD4+CD25+FoxP3+调节T细胞明显高于患者及健康人群外周血。在体外,结核性胸膜炎患者胸液中单核细胞对BCG刺激产生γ-干扰素(IFN-γ)的能力明显强于患者及健康人群外周血中单核细胞;把这些调节T细胞从胸液单核细胞中清除,增强了结核患者胸液单核细胞对BCG刺激产生IFN-γ;从结核患者胸液分离的这些调节T细胞能抑制结核患者Th1细胞产生IFN-γ。结论结核性胸膜炎患者胸液CD4+CD25+FoxP3+调节T细胞增多,抑制结核性胸膜炎患者Th1细胞免疫反应,从而参与了结核性胸膜炎的发病。     

人类免疫缺陷病毒和丙型肝炎病毒重叠感染者的临床及免疫特征

目的 观察人类免疫缺陷病毒(HIV)和HCV重叠感染者与慢性丙型肝炎患者临床特征及HCV特异性细胞毒性T淋巴细胞(CTL)的数量及功能,探讨两组患者免疫功能的差异及其可能的影响因素.方法 以HIV和HCV重叠感染患者59例、慢性丙型肝炎患者36例为研究对象,取治疗前外周血检测肝脏生物化学指标、血常规、外周血T淋巴细胞亚群(CD4+T、CD8+T淋巴细胞计数)及HIV、HCV病毒载量,以酶联免疫斑点法检测HCV特异性CTL的数量和功能,统计学分析两组问免疫功能的差异及与上述检测指标的相关性. 结果 中国河南省有偿献血、单采血浆人群HIV感染者中HIV和HCV重叠感染率达60.8%.ALT、AST值在重叠感染组与HCV组间差异无统计学意义;球蛋白在重叠感染组为(40.3±5.8)g/L,HCV组为(32.8±6.3)g/L,差异有统计学意义(P＜0.01).重叠感染组外周血CD4+T淋巴细胞数明显低于HCV组(P＜0.01),而CD8+T淋巴细胞数高于HCV组(P＜0.01).重叠感染组HCV RNA定量高于HCV组(P＜0.01).重叠感染组对HCV-NS3区肽段的反应强度(每106个外周血单个核淋巴细胞中斑点形成细胞的个数)较HCV组弱,649.34±685.90对比1233.70±1085.16,差异有统计学意义(P＜0.05).重叠感染组白蛋白与HCV病毒载量呈现负相关(r=0.540);重叠感染组对HCV-NS3区肽段反应强度与HIV病毒载量负相关(r=0.356);重叠感染患者CD4+T淋巴细胞数与血小板正相关(P＜0.05).但未见重叠感染组HCV RNA与CD4+T淋巴细胞数量及HIVRNA水平有相关关系.结论 重叠HIV感染有利于HCV的复制,而HIV载量可影响针对HCV的特异性免疫反应,HIV载量高则不利于HCV的清除.慢性丙型肝炎患者重叠HIV感染时,病情易慢性化,预后更差.     

HIV急性期/早期感染者合并HBV感染的临床特征

目的探讨艾滋病病毒(HIV)急性期/早期感染者合并感染乙型肝炎病毒(HBV)的临床特点及实验室特征,进一步明确影响HIV/HBV重叠感染疾病进展的关键因素。方法采用回顾性分析的方法,了解单独HIV急性期/早期感染者(单独HIV感染组)和合并HBV的HIV急性期/早期感染者(HIV/HBV重叠感染组)的初始CD+4T淋巴细胞(简称CD4细胞)计数和病毒载量调定点,以及两组病人感染HIV一年内CD4细胞计数和HIV病毒载量的动态变化,和HIV急性期/早期合并HBV感染的临床特征。结果 20例HIV/HBV重叠感染组的初始CD4细胞计数平均值为(443.55±197.00)个/μL(213~985个/μL),病毒载量调定点(4.34±0.99)Log10拷贝/mL(1.82~5.47Log10拷贝/mL)。30例单独HIV感染组病人的初始CD4细胞计数平均值为(497.37±121.29)个/μL(196~792个/μL),病毒载量调定点(3.87±0.62)Log10拷贝/mL(2.77~5.19Log10拷贝/mL)。HIV/HBV重叠感染组的初始CD4细胞计数明显低于单独HIV感染组,两组比较差异有统计学意义(P0.05)。HIV/HBV重叠感染组的病毒载量调定点明显高于单独HIV感染组,两组间差异有统计学意义(P0.05)。结论在我国HIV急性期/早期感染者中,HIV/HBV重叠感染者与单独HIV感染者比较,初始CD4细胞计数明显降低,病毒载量调定点明显升高,HIV病毒复制更为活跃。     

腹主动脉瘤患者外周血CD19~+CD24~(hi)CD38~(hi)B细胞功能变化

目的观察腹主动脉瘤(AAA)患者外周血CD4 T细胞比例及干扰素(IFN)-γ分泌情况,以及CD19+CD24hiCD38hiB调节性B细胞(Breg)比例及功能的变化情况。方法采用流式细胞术测定40例AAA患者及同期入院进行健康体检者外周血CD4 T细胞、IFN-γ+CD4 T细胞和CD19+CD24hiCD38hiB细胞比例;采用CFSE染色方法检测CD19+CD24hiCD38hiB细胞对CD4 T细胞增殖能力的影响;采用流式细胞术测定CD19+CD24hiCD38hiB细胞与CD4 T细胞共孵育后对CD4 T细胞分泌IFN-γ的影响。结果 AAA患者外周血CD4 T细胞比例显著升高(P0.05)。与健康对照相比,AAA患者外周血IFN-γ+CD4 T细胞比例亦升高(P0.01);AAA患者与HC外周血CD19+CD24hiCD38hiB细胞比例比较,差异不具有统计学意义(P0.05);健康对照外周血CD19+CD24hiCD38hiB细胞可显著抑制CD4 T细胞增殖和IFN-γ分泌能力,而AAA患者外周血CD19+CD24hi CD38hiB细胞不具有此功能。结论 AAA患者外周血CD19+CD24hiCD38hiB细胞功能的丧失,致使外周血CD4 T细胞比例升高和IFN-γ分泌的能力增强,最终导致AAA的发生和发展。     

人类免疫缺陷病毒与重叠丙型肝炎病毒感染者免疫指标比较

目的 分析HIV/HCV重叠感染人群与HIV单独感染人群治疗前临床特征及免疫功能的差异,探讨其可能的影响因素.方法 以HIV/HCV重叠感染患者59例、HIV单独感染患者38例为研究对象,取患者治疗前外周血,检测其肝功能、血常规、外周血T细胞亚群(CD4+、CD8+)及HIV、HCV病毒载量,酶联免疫斑点法(ELISPOT)检测HIV特异性细胞毒性T淋巴细胞(CTL)的数量和功能.结果 HIV/HCV重叠感染率达60.8%.重叠感染组ALT、AST均明显高于HIV组(49.8 U/L比23.6 U/L,49.1 U/L比32.3 U/L,P值分别为0.000、0.013);重叠感染组PLT明显低于HIV组[(167.3±59.2)×109/L比(198.0±63.9)×109/L,P=0.040].外周血T细胞亚群检测结果两组间差异无统计学意义.重叠感染组HIV RNA定量为(4.046±0.541)lOglo拷贝/mL,低于HIV组的(4.394±0.507)log10拷贝/mL(P=0.018).重叠感染组对HIV-Gag全序列肽段的阳性孔斑点数(平均秩次30.85)较HIV组(平均秩次44.34)低,阳性孔数(4.60±5.52)低于HIV组(6.24±6.93),但两组比较差异无统计学意义.重叠感染组Alb与HCV病毒载量呈负相关(r=-0.540),CD4+与PLT呈正相关(P=0.000).结论 单采血浆感染HIV患者中,有较高的HIV/HCV重叠感染率和较低的细胞免疫功能.     

抗病毒治疗对慢性丙型肝炎CD4^＋CD25^＋调节性T细胞频率和功能的影响

目的研究抗病毒治疗前后慢性丙型肝炎患者CD4^＋CD25^＋调节性T细胞（Treg）频率和功能的变化。方法筛选HLA—A2阳性慢性丙型肝炎患者31例，给予聚乙二醇化干扰素α-2a（相对分子质量为40000）180μg每周1次皮下注射，联合口服利巴韦林。分别在治疗前和治疗结束随访24周时应用流式细胞仪检测患者CD4^＋CD25^＋ Treg细胞占外周血CD4^＋T细胞的频率，应用液闪计数仪检测其对HCV特异性CD8^＋T细胞增殖的抑制作用，ELISA法检测细胞培养上清γ干扰素（IFN-γ）水平的变化情况。结果治疗结束随访24周，患者外周血CD4^＋CD25^＋ Treg细胞频率为（9．6±3．0）％，明显低于治疗前的（11．0±2．3）％（t=2．028，P〈0．05）；持续病毒学应答（SVR）组CD4^＋CD25^＋ Treg细胞频率为（8．9±2．7）％，明显低于未获得SVR患者组的（10．4±2．3）％（t=3．324，P〈0．01）。抗病毒治疗后CD4^＋CD25^＋ Treg细胞抑制HCV特异性CD8^＋T细胞增殖的作用减弱。治疗后患者IFN-γ水平为（3959±577）pg／ml，明显高于治疗前的（1965±326）pg／ml（t=16．1，P〈0．01）；获得SVR患者组IFN-γ（6824±568）pg／ml，明显高于未获得SVR患者组的（2219±286）pg／ml（t=29．853，P〈0．001）。结论慢性丙型肝炎患者随着HCV RNA水平的下降，CD4^＋CD25^＋Treg细胞频率降低，抑制HCV特异性CD8^＋T细胞增殖的作用减弱。     

慢性乙型肝炎外周血中T细胞亚群和NK细胞的变化及临床意义

目的观察慢性乙型肝炎患者外周血中T细胞亚群及NK细胞含量的变化,进一步了解慢性乙型肝炎患者的免疫功能状况。方法收集48例慢性乙型肝炎患者作为实验组,其中HBe Ag阳性20例,阴性28例,选择26名健康人群作为正常对照组,采用流式细胞仪检测两组血清中CD3+T细胞、CD4+T细胞、CD8+T细胞和NK细胞的含量。结果与正常对照组比较,慢性乙型肝炎患者外周血中CD3+T细胞、CD4+T细胞和NK细胞的含量明显降低,而CD8+T细胞含量升高,差异具有统计学意义(P0.05),而HBe Ag阳性和阴性的慢性乙型肝炎患者之间的差异无统计学意义(P0.05)。结论慢性乙型肝炎患者免疫功能低下,这对患者免疫功能的判断、疾病进展、治疗及预后有一定的指导意义。     

扩张型心肌病患者CD4~+CD25~+Foxp3~+ T细胞的检测及意义

目的:探讨扩张型心肌病(DCM)患者外周血CD4+CD25+Foxp3+T细胞的水平及意义。方法:采用流式细胞术检测DCM患者30例及健康对照组20例外周血CD4+CD25+T细胞和CD4+CD25+Foxp3+T细胞的比例。结果:DCM患者外周血CD4+CD25+T细胞占CD4+T细胞的比例为(8.53±1.64)%,显著低于健康对照组的(11.4±2.17)%,P0.01;DCM患者CD4+CD25+Foxp3+T细胞占CD4+T细胞比例为(0.99±0.54)%,显著低于健康对照组的(1.55±0.55)%,P0.01;且DCM患者心功能越差,CD4+CD25+Foxp3+T细胞占CD4+T细胞的比例越低。结论:DCM患者调节性T细胞比例的减少,可能打破了自身免疫耐受,发生了针对心肌抗原的自身免疫反应,参与了DCM的发病。     

Detection of intracellular IFN‐γ and IL‐4 cytokines in CD4+ and CD8+ T cells in the peripheral blood of dogs naturally infected with Leishmania infantum

Canine leishmaniosis (CanL) is a systemic zoonotic disease the clinical manifestations of which can range from self‐healing cutaneous lesions to disseminated visceral disease. Effective activation of cellular immunity is the cornerstone of resistance against Leishmania infantum in infected dogs. The aim of this cross‐sectional, controlled study was the intracellular detection of interleukin 4 (IL‐4) and interferon‐γ (IFN‐γ) in CD4+ and CD8+ lymphocytes in the peripheral blood of 40 dogs naturally infected with L. infantum by applying flow cytometry. The percentage of CD4+IL‐4+ and CD8+IL‐4+ lymphocytes (with or without immunostimulation) was low in the clinically healthy and subclinically infected dogs in contrast to clinically affected ones. In the same groups of dogs, the percentage of CD4+IFN‐γ+ and CD8+IFN‐γ+ T cells in their resting phase and following specific immunostimulation with Leishmania soluble antigen (LSA) was also low. CD4+IL‐4+ and CD8+IL‐4+ T cell percentage was higher in sick compared to clinically healthy and subclinically infected dogs, after immunostimulation. The corresponding figure of CD8+IL‐4+ cells in sick dogs after LSA immunostimulation was also increased thus underlining the important role these cells may play in humoral immunity and perhaps the progression of CanL.     

肺结核患者外周血CD_4~+、CD_8~+T细胞Blimp-1表达下降

目的研究活动性肺结核患者外周血单个核细胞(PBMCs)Blimp-1的表达及临床意义。方法采集31例活动期肺结核患者和45位健康对照组外周血,纯化PBMCs,用结核分枝杆菌ESAT-6和CFP-10混合性抗原肽库刺激,通过细胞表面标记和细胞内细胞因子染色技术,采用流式技术检测CD+4、CD+8T细胞Blimp-1的表达。结果与对照组比较,肺结核患者PBMCs中的CD+4、CD+8T细胞亚群分布出现显著性下降,且肺结核患者CD+4T细胞中Blimp-1的表达比例(%)下降(肺结核组89.5%(83.8%,95.7%),对照组94.5%(89.8%,98.7%),P0.05),且CD+4、CD+8T细胞中Blimp-1的表达量(平均荧光强度)也显著性下降(CD+4T细胞:肺结核组9.28(7.5,18.9),对照组15.4(11,25.4),P0.05);CD+8T细胞:肺结核组9.01(6.08,14.7),对照组14.2(9.53,23.1),P0.05)。结论活动期肺结核CD+4、CD+8T细胞群内Blimp-1的表达下降可能会使效应性和调节性T细胞的分化出现异常。Blimp-1可能参与结核病的疾病进程,这为研究结核病的诊断和治疗提供了线索。     

Cytokine activity after allogeneic bone marrow transplantation, V. Analysis of IL-2 and IFN production by isolated CD4+ and CD8+ cells

Summary. Previous studies from this laboratory have shown that PBMC from recipients of an HLA-identical sibling bone marrow transplant produce levels of IL-2 which are 10–100-fold lower than those produced by the same number of PBMC from healthy controls, whereas production of IFN-γ is normal. The present study examined IL-2 and IFN production over a range of cell numbers for PBMC and for isolated CD4⁺ and CD8⁺ cells for controls and marrow transplant recipients. There was a 5-fold lower IL-2 production in marrow transplant recipient CD8⁺ cells compared with equivalent numbers of control cells, whereas no difference was found in IL-2 production by CD4⁺ cells. In contrast, IFN production by CD4⁺ cells from marrow transplant recipients was 4-fold higher than in controls, whereas CD8⁺ cells from both populations produced similar amounts of IFN. When the observed production of cytokine by PBMC was compared with the expected production based on the CD4⁺ and CD8⁺ content of the PBMC, control values were similar, but the expected values for both cytokines were approximately 2-fold higher than the observed values for marrow transplant recipients. The results suggest that the capacity of T cells from marrow transplant recipients to produce IL-2 and IFN is not impaired, but that the frequency of cytokine-producing cells may be reduced, and that a negative interaction present in recipient PBMC, eliminated by isolating T-cell subsets, is responsible for the observed low levels of cytokine production.     

Idiotype-specific T lymphocytes in monoclonal gammopathies: evidence for the presence of CD4+ and CD8+ subsets

Tumour-specific CD4⁺ T helper (Th) and CD8⁺ T cytotoxic (Tc) cells may participate in the control and eradication of tumour cells. In the present study, idiotype-specific stimulation of CD4⁺ and CD8⁺ blood T cells from patients with monoclonal gammopathy of undetermined significance and patients with untreated multiple myeloma stage I was examined. Activation was measured in the CD4⁺ and CD8⁺ subsets enriched by magnetic microbeads as the incorporation of ³H-thymidine and the secretion of interferon (IFN)-γ, interleukin (IL)-2 and IL-4 by single cells using the enzyme-linked immunospot assay. Idiotype-specific T cells were found in four of seven patients. Stimulation was mainly confined to the CD4⁺ subset in three of the four responding patients. This type of response was major histocompatibility complex (MHC) class II restricted as it could be inhibited by monoclonal antibodies against MHC class II (HLA-DR), but not against class I (HLA-ABC) molecules. Idiotype-specific CD8⁺ T cells were also demonstrated in these patients although at a lower frequency. One patient showed a strong and dominating activation of CD8⁺ T cells which could be blocked by antibodies against HLA-ABC but not against HLA-DR. Idiotype-specific CD4⁺ or CD8⁺ T cells were mainly of the type-1 subsets as judged by their secretion of IFN-γ and IL-2. Thus, this study provides evidence for the presence of idiotype-specific and MHC-restricted CD4⁺ and CD8⁺ T cells of the type-1 subsets in patients with monoclonal gammopathies. Such T cells with the potential to control the growth of tumour B cells may be a suitable target for immunotherapeutic interventions in patients.     

COPD相关T淋巴细胞亚群的新功能

肺部慢性非特异性炎症被认为是COPD发生发展的病理基础,淋巴细胞在调节 COPD气道炎症中发挥重要的作用.研究发现,效应T细胞、抑制性 T细胞与耗竭 T细胞三者在 COPD的炎症调节中发挥着不同的正负调节效应,它们分化上互相关联,功能上互相拮抗,一旦发生免疫失衡,可加重气道结构的破坏、加速COPD的进展和恶化.     

支气管哮喘大鼠CD4+CD25+T细胞的变化及地塞米松干预作用的研究

目的 研究支气管哮喘(简称哮喘)大鼠模型支气管肺泡灌洗液(BALF)、血液、脾脏CD4+CD25+T细胞的变化,及地塞米松对CD4+CD25+T细胞的影响.方法 50只SD大鼠随机分为5组,空白对照(A)组,哮喘(B)组,地塞米松1(C)组、地塞米松2(D)组,地塞米松3(E)组.A组第l天给予腹腔注射生理盐水l ml,第15～21天每天给予生理盐水雾化.B、C、D、E组用卵蛋白建立哮喘大鼠模型,第1天,每只大鼠腹腔注射抗原l ml(卵蛋白1 mg+灭活百日咳杆菌9×106个+氢氧化铝干粉100 mg)混悬液,第15～21天给予1%的卵蛋白雾化30 min,C、D、E组于雾化后分别给予腹腔注射地塞米松0.2 mg/kg、1 mg/kg、2 mg/kg.采用流式细胞仪检测的方法 ,观察大鼠体内BALF、外周血、脾脏CD4+CD25+T细胞的变化及使用不同剂量地塞米松后对其的影响.结果 B组BALF、外周血、脾脏CD4+CD25+T细胞表达占CD4+T细胞的百分比分别是(42.21±5.62)%、(12.69±2.70)%、(11.15±1.05)%,A组结果 分别是(18.76±5.85)%、(6.21±1.73)%、(7.85±2.13)%.B组与A组比较,差异均具有统计学意义(P＜0.01,P＜0.01,P＜0.05);C组、D组、E组BALF中CD4+CD25+T细胞占CD4+T细胞的百分比表达分别是(10.49±4.03)%、(13.28±5.12)%、(7.51±5.39)%,显著低于A组和B组,(P＜0.05,P＜0.01);外周血中,C组(6.03±1.43)%、D组(4.88±0.95)%与A组(6.21±1.73)%比较,差异无统计学意义,E组(3.49±0.62)%与C组、A组比较,差异有统计学意义(P＜0.05).脾脏中,C组(7.25±1.82)%、D组(8.63±3.18)%与A组(7.85±2.13)%比较,差异无统计学意义,E组(3.38±1.37)%与C组、D组、A组比较,差异有统计学意义(P＜0.05).结论 CD4+CD25+T细胞在哮喘大鼠体内有明显的优势表达,可能是哮喘发病的机制之一.地塞米松可以抑制CD4+CD25+T细胞的表达.BALF内CD4+CD25+T细胞的变化与外周血和脾脏的变化具有一致性,监测外周血或脾脏CD4+CD25+T细胞变化可了解肺部情况.     

增龄对人体外周血CD4+CD25+Foxp3+调节T细胞、CD4+T细胞及细胞因子表达的影响

目的探讨增龄对人体外周血CD4⁺CD25⁺Foxp3⁺调节T细胞(CD4⁺CD25⁺Foxp3⁺Treg)、CD4⁺T细胞及细胞因子表达的影响。方法选择青年人(20~45岁)、中老年人(50~75岁)及高龄老年人(≥80岁)各40例,分别检测3组外周血CD4⁺T、CD4⁺CD25⁺Foxp3⁺Treg的绝对计数,并计算后者占前者的百分比,同时检测并比较3组人群外周血IL-2、干扰素-γ(IFN-γ)、TNF-α、IL-10和IL-17水平。结果高龄老年组CD4⁺T细胞绝对计数较中老年组与青年组显著下降(P<0.05);高龄老年组和中老年组外周血CD4⁺CD25⁺Foxp3⁺Treg绝对计数均明显高于青年组(P<0.05);中老年组CD4⁺CD25⁺Foxp3⁺Treg占CD4⁺T细胞百分比明显高于青年组,高龄老年组明显高于中老年组,差异均有统计学意义(P<0.05)。高龄老年组IL-2、IFN-γ和IL-17水平明显低于青年组和中老年组(P<0.05),中老年组IL-2明显低于青年组(P<0.05),高龄老年组IL-10水平明显高于青年组和中老年组(P<0.05),3组TNF-α水平差异无统计学意义(P>0.05)。结论中老年以后人体外周血CD4⁺CD25⁺Foxp3⁺Treg绝对计数明显增高,随着增龄,其占CD4⁺T细胞百分比逐渐升高。高龄老年人外周血CD4⁺T细胞绝对计数、IL-2、IFN-γ和IL-17水平明显下降,IL-10水平明显增高,说明老年人免疫功能进一步下降,衰老的微环境发生了改变。     

Mouse splenic CD4+ and CD8+ T cells undergo extensive apoptosis during a Plasmodium chabaudi chabaudi AS infection

The presence and phenotype of apoptotic lymphocytes was studied in spleen cell suspensions taken from CB6F1 mice infected with Plasmodium chabaudi chabaudi AS. High levels of apoptotic cells were found, associated with high parasitaemias and splenomegaly. This was also accompanied by expansion and disarray of spleen white pulp. Apoptosis levels lowered when parasitaemia was cleared, but were still higher than in normal mice. At this time, the spleen was diminishing in size and the white pulp was contracting and rearranging. When parasitaemia was patent, the cells most affected by apoptosis were CD4+ T cells followed by CD8+ T cells, and to a lesser extent B220+ B cells. When parasitaemia was cleared, CD8+ T cells and B220+ B cells returned to basal levels of apoptosis, while CD4+ T cells still had higher apoptosis levels than normal mice. A similar pattern of lymphocyte subpopulation apoptosis was found in infected BALB/c mice, despite the fact that, for this mouse model, it has been reported that B cells are the cells that are most affected by apoptosis. We consider that the high levels of apoptosis in CD4+ T cells when parasitaemias are still high are not easily explained by a normal mechanism of down regulation of the immune response.