从CD4+CD25-Foxp3+ T细胞变化看系统性红斑狼疮外周免疫耐受失衡

目的: 检测CD4+CD25-Foxp3+ T细胞在系统性红斑狼疮(SLE)患者外周血中的表达,探讨该细胞亚群在SLE发病机制中的意义.方法: 采用流式细胞术检测25例SLE患者和15例健康对照的外周血CD4+CD25-Foxp3+ T细胞比例、分析其表型;利用免疫磁珠细胞分选法(MACS)分选出CD4+CD25-T细胞,通过实时定量聚合酶链反应(real-time PCR)检测FOXP3基因表达.结果: 活动期和稳定期SLE患者外周血CD4+CD25-Foxp3+ T细胞比例分别是: (9.89 ±0.85)%和(7.11±0.86)%,与健康对照组 (3.35±0.31)% 比较差异有统计学意义(P<0.01).SLE患者CD4+CD25-Foxp3+ T细胞表达频率与SLEDAI评分呈明显正相关(P=0.0008).活动期SLE患者CD4+CD25-T细胞中Foxp3在蛋白和基因转录水平上的表达均高于健康对照组(P<0.01).SLE患者CD4+CD25-Foxp3+ T细胞表面低表达CD127.结论: SLE患者外周血中CD4+CD25-Foxp3+ T细胞比例变化可能反应了SLE发病中T细胞外周免疫失耐受机制"调节性T细胞的抑制效应被抵抗".     

Caspase-8信号分子对SLE患者T细胞亚群的双向调节作用研究

目的 分析SLE患者外周血T细胞内活化Caspase-8、Caspase-3和T细胞膜上Fas、CD69以及外周血中Foxp3 CD4 CD25 调节性T细胞的表达,探讨他们在SLE患者免疫失衡中的作用.方法 用流式细胞术检测活化Caspase-8、Caspase-3和Fas、CD69以及Foxp3 CD4 CD25 Treg的表达.结果 与健康对照相比,SLE患者外周血CD3 CD4 T细胞上Fas表达显著升高(P＜0.05),无论稳定期或活动期SLE患者CD3 CD4 T细胞和CD3 CD8 T细胞中活化Caspase-8的表达均显著增加(P＜0.05),且稳定期和活动期SLE患者CD3 CD8 T细胞中活化Caspase-8的表达高于其在CD3 CD4 T细胞中的表达(P＜0.05);但是仅活动期SLE患者T细胞内活化Caspase-3表达增加(P＜0.05),同时稳定期和活动期SLE患者CD3 CD4 T细胞中活化Caspase-3的表达高于其在CD3 CD8 T细胞中的表达(P＜0.05).同时SLE患者CD3 CD8 T细胞上CD69表达率升高(P＜0.05),但是CD69在CD3 CD4 T细胞上的表达率与健康对照相比无显著性差异(P＞0.05).SLE患者外周血中Foxp3 CD4 CD25 Treg比例显著低于健康对照(P＜0.05).结论 Caspase-8介导的信号事件同时参与诱导SLE患者淋巴细胞的凋亡与活化,促使SLE患者体内免疫反应向Th2极化,同时由于SLE患者外周血中Foxp3 CD4 CD25 Treg表达降低所介导的免疫抑制效应缺陷,他们共同作用促使SLE患者外周免疫平衡障碍.     

CD4+CD25+调节性T细胞与系统性红斑狼疮病情活动性关系的研究

目的：检测系统性红斑狼疮患者外周血CD4^＋CD25^＋、CD4^＋CD8^＋调节性T细胞亚群，探讨其与疾病活动性、肾脏损伤、血清抗ds-DNA抗体及免疫球蛋白和补体C3含量的关系。方法：采用流式细胞术检测北京协和医院住院和门诊SLE患者（n=37）外周血CD4^＋CD25^＋T、CD4^＋CD8^＋T细胞群比例，以15例RA和15例SS组成自身免疫性疾病对照，30例健康体检者作为正常对照，观察调节性T细胞亚群与SLE患者疾病活动性指标SLEDAI、IgG、C3及血清抗ds-DNA抗体的关系。结果：①疾病活动期SLE患者外周血CD4^＋CD25^＋调节性T细胞群比例显著低于正常对照组（P〈0.01），疾病稳定期和风湿性疾病对照组与正常对照组结果差异无统计学意义。疾病活动期和稳定期SLE患者CD4＋CD8＋T细胞群比例都略高于正常对照组，但未发现结果差异有统计学意义（P〉0.05）。②疾病活动期SLE患者外周血CD4^＋CD25^＋T细胞比例及CD4^＋CD25^＋/CD4^＋值显著低于稳定期患者（P〈0.01）。SLE患者外周血CD4^＋CD25^＋/CD4^＋值与SLEDAI、补体C3呈低度相关（r分别为-0.491、0.368，P〈0.05），CD4^＋CD25^＋T细胞数量与SLEDAI呈负相关（r=-0.578，P〈0.05）。③SLE并发肾病组外周血CD4^＋CD25^＋T细胞群比例及CD4^＋CD25^＋/CD4^＋值显著低于非肾病组（P〈0.01；P〈0.05）。同一SLE患者治疗前后CD3^＋CD4^-CD8^-细胞和NK细胞降低，CD4^＋CD25^＋细胞、CD4^＋CD25^＋/CD4^＋值及CD8^＋T细胞增加，但未发现这些结果差异有统计学意义。本次研究未发现NK细胞、CD4^＋CD8＋T细胞、CD4^＋CD25^＋T细胞群比例在ds-DNA＋组与ds-DNA-组之间结果差异有统计学意义。结论：SLE患者外周血CD4^＋CD25^＋T细胞群比例与SLEDAI成负相关，与肾脏的损害也有密切关系，但与血清抗ds-DNA抗体产生的关系不明显。活动期SLE患者外周血CD4^＋CD25^＋T细胞减少，稳定期CD4^＋CD25^＋T细胞比例回升，因此推测CD4^＋CD25^＋T细胞的变化可能是导致疾病发生和病情发展及相关器官（如肾脏）损伤的关键环节之一。     

类风湿性关节炎患者CD4+CD25+Foxp3+调节性T细胞检测及意义

目的:研究CD4 CD25 FoxP3 调节性T细胞在类风湿关节炎患者(RA)外周血中的比例改变,并探讨其在疾病进程中的意义.方法:选取活动期及稳定期RA患者,采用细胞内染色的流式细胞术及定量PCR的方法,分别在蛋白质和mRNA水平检测FoxP3表达,并与正常人进行比较.结果:RA患者CD4和CD25双阳性细胞所占比例与对照组没有明显差异,而活动期患者外周血CD4 CD25high和CD4 CD25 FoxP3 细胞明显低于稳定期和对照组(P＜0.05).FoxP3 mRNA表达水平与蛋白质表达水平变化相一致.结论:类风湿性关节炎活动期时CD4 CD25 FoxP3 调节性T细胞明显减少,这群调节性T细胞可能参与了类风湿性关节炎的病理进程.     

CD4+CD25+调节性T细胞在川崎病免疫发病机制中的作用

目的探讨CD4 CD25 调节性T细胞在川崎病(KD)免疫发病机制中的作用。方法急性期KD患儿25例,正常同年龄对照组25例,KD患儿分别于静脉丙种球蛋白(IVIG)治疗前后直接取血备检,未加任何体外丝裂原刺激培养。采用流式细胞术分别检测外周血CD4 CD25 调节性T细胞比例及CD14 细胞表面共刺激分子的表达;逆转录-聚合酶链反应(RT-PCR)及荧光定量PCR检测外周血CD4 T细胞中Foxp3、CTLA-4和GITR基因mRNA的表达。结果急性期KD患儿外周血CD4 CD25 调节性T细胞比例明显低于同年龄对照组(P<0.01),IVIG治疗后显著上升(P<0.01);急性期KD患儿外周血CD4 T细胞中Foxp3、CTLA-4和GITR基因mRNA表达水平均明显低于正常对照组(P<0.01),IVIG治疗后均有不同程度的恢复(P<0.01);急性期KD患儿CD14 细胞明显过度表达CD80及CD86等共刺激分子(P<0.01),IVIG治疗后CD80及CD86表达均显著下降。结论急性期KD患儿CD4 CD25 调节性T细胞数量减少可能与KD免疫调节功能紊乱有关。     

CD4+CD25+Treg在急性淋巴细胞白血病患者外周血中的表达及其体外实验研究

目的初步探讨CD4 CD25 调节性T细胞(CD4 CD25 regulatory T cells,CD4 CD25 Treg)在急性淋巴细胞白血病(acute lymphocytic leukemia,ALL)患者化疗前及化疗缓解后外周血中的表达水平,并研究患者血清能否诱导外周血CD4 CD25-T细胞转化为CD4 CD25 Treg。方法①采用流式细胞术分别检测ALL初诊组、化疗完全缓解或部分缓解组及正常对照组外周血中CD4 CD25 T细胞所占比例,然后通过荧光定量RT-PCR检测各组外周血中转录因子Foxp3mRNA的表达水平,并逐层分析比较。②采集正常人外周血单个核细胞后,对照组用正常人血清,实验组用患者血清并分别设浓度梯度进行培养,72h后采用流式细胞术、荧光定量RT-PCR分别检测CD4 CD25 T细胞和Foxp3mRNA表达。结果ALL化疗缓解组CD4 CD25 T细胞及Foxp3mRNA表达水平均明显高于ALL初诊组和正常对照组(P<0.05),后两者之间CD4 CD25 T细胞水平无统计学差异(P>0.05),但ALL初诊组Foxp3mRNA含量较正常对照组明显升高(P<0.01),差异具有统计学意义;并且血清培养对照组CD4 CD25 T细胞水平及Foxp3mRNA含量均明显低于实验组(P<0.05),且其表达并不随血清浓度的增加而升高。结论CD4 CD25 Foxp3 Treg在ALL初诊组及化疗缓解组患者外周血中比例明显升高,且初步表明患者血清中的可溶性物质可诱导外周血CD4 CD25 T细胞转化为CD4 CD25 Treg,提示CD4 CD25 Treg可能是ALL免疫抑制的一个重要原因。     

系统性红斑狼疮患者CD4+T细胞上CD137的表达

目的:探讨系统性红斑狼疮(Systemic lupus erythematosus,SLE)患者CD4 T细胞上共刺激分子CD137的表达及其作用机制。方法:应用流式细胞术检测30例系统性红斑狼疮患者和20例正常对照者外周血T细胞活化前后CD137的表达。结果:活动期SLE患者CD4 T细胞表达的CD137明显高于稳定期及正常对照组(表达百分率分别为21.56±4.08、3.01±0.09和1.24±0.12,P<0.01),稳定期SLE患者表达的CD137与正常对照组比较无统计学差异(P>0.05)。但是活动期和稳定期SLE患者的CD4 T细胞用抗CD3单抗体外刺激活化后表达的CD137均显著高于正常对照组(表达百分率分别为56.25±9.11、27.26±3.41和13.17±1.54,P<0.01)。另外,活动期SLE患者CD4 T细胞活化后表达的CD137与补体呈负相关关系(r=-0.447,P<0.05),与IgG和24小时尿蛋白定量呈正相关关系(r=0.451,P<0.05,r=0.245,P<0.05)。结论:活动期系统性红斑狼疮患者T细胞活化前后CD137的表达均显著增高,而且CD4 T细胞活化后CD137表达水平可能提示病情和肾脏受累程度。     

RA患者外周血CD8＋CD28-和CD4＋CD25＋调节性T细胞的表达及疾病活动性指标相关性分析

目的：检测类风湿性关节炎（RA）患者外周血CD8＋CD28-、CD4＋CD25＋调节性T细胞亚群,探讨其与临床活动性指标的关系。方法：采用流式细胞术检测台州医院RA患者外周血CD8＋CD28-、CD4＋CD25＋ T细胞亚群比例,探讨调节性T细胞与RA活动性、类风湿因子（RF）、免疫球蛋白（Ig）、C反应蛋白（CRP）、补体C3、抗CCP抗体、抗核抗体（ANA）、血小板（PLT）及血沉（ESR）的关系。结果：活动期RA患者外周血CD4＋CD25＋调节性T细胞亚群比例显著低于正常对照组（P〈0.01）,但稳定期RA患者与正常对照组结果差异无统计学意义（P〉0.05）。活动期和稳定期RA患者CD8＋CD28-与正常对照组相比较,结果无统计学意义（P〉0.05）;CD4＋CD25＋与CRP密切相关（r=-0.593,P〈0.05）,CD8＋CD28-与ESR相关系数呈弱相关。CD4＋CD25＋和CD8＋CD28-细胞与RF、IGG、C3、ANA、anti-CCP和PLT未见明显相关性。结论：活动期RA患者外周血CD4＋CD25＋ T细胞亚群比例减少,CD4＋CD25＋ T细胞可能与类风湿性关节炎疾病进展有关。     

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。     

Graves病患者131I治疗前后CD4+CD25+ Foxp3+调节性T细胞的变化

目的:通过对Graves病患者131I治疗前后外周血各淋巴细胞亚群和CD4+CD25+ Foxp3+调节性T细胞含量以及相关基因Foxp3mRNA表达水平的测定,探讨131I治疗方法是否可以通过改变调节性T细胞的含量从而改善Graves病患者的免疫功能异常。方法:采集30例Graves病患者131I治疗前及治疗后1个月的外周血,流式细胞仪检测外周血CD3+、CD3+CD4+、CD3+CD8+、CD3-CD19+、CD3-CD16+CD56+淋巴细胞亚群及CD4+CD25+ Foxp3+调节性T细胞的百分率,Real-TimePCR检测外周血单个核细胞Foxp3mRNA的表达水平。结果:和治疗前相比,Graves病患者131I治疗1个月后外周血CD3+CD4+T细胞和CD3-CD19+B细胞百分率都明显减少(P<0.05),CD3-CD16+CD56+NK细胞百分率明显增加(P<0.05),CD3-CD8+T细胞、CD4+CD25+ Foxp3+调节性T细胞百分率和Foxp3mRNA的表达水平无明显变化。结论:131I不能通过增加调节性T细胞的含量而改善Graves病患者的免疫耐受障碍,但可以通过减少CD4+T和B淋巴细胞的含量和增加NK细胞的含量来控制过度的免疫应答。     

Inverse correlation between CD4+ regulatory T-cell population and autoantibody levels in paediatric patients with systemic lupus erythematosus

CD4(+) CD25(+) regulatory T cells (Tregs) are critical in maintaining self-tolerance and preventing organ-specific autoimmunity. Their role in paediatric systemic lupus erythematosus (SLE), an autoimmune disease characterized by inappropriate regulation of hyperactivated B and T cells, has not been clearly defined. Using flow cytometry to determine cell populations and real-time polymerase chain reaction to assay mRNA expression for FOXP3, CTLA-4, and GITR, we characterized CD4(+) CD25(+) T cells in paediatric SLE patients and healthy subjects. The frequency of CD4(+) CD25(+) Tregs was significantly decreased in patients with active SLE compared with patients with inactive SLE and with controls (7.27% +/- 2.50%, 9.59% +/- 2.80% and 9.78% +/- 2.11%, respectively; P = 0.027 and P < 0.001, respectively), and was inversely correlated with disease activity, as assessed with the Systemic Lupus Erythematosus Disease Activity Index 2000 scores (r = -0.59, P = 0.001) and serum anti-double-stranded DNA levels (r = -0.65, P < 0.001). Our preliminary investigations found elevated surface expression of GITR in CD4(+) CD25(+) T cells, elevated mRNA expression of CTLA-4 in CD4(+) T cells and higher amounts of mRNA expression for FOXP3 in CD4(+) cells in patients with active SLE compared with patients with inactive disease and controls. We demonstrated reduced CD4(+) CD25(+) Treg levels were inversely correlated with disease activity, indicating a defective Treg population in paediatric SLE patients. The differences in the expression of FOXP3, CTLA-4 and GITR imply the possible role of CD4(+) Tregs in the pathogenesis of SLE.     

卵巢癌细胞培养上清诱导CD4+CD25-T细胞分化为CD4+CD25+调节性T细胞

目的研究卵巢癌细胞培养上清液是否能诱导外周血CD4^＋CD25^- T细胞转变为CD4^＋CD25^＋调节性T细胞。方法将外周血CD4^＋CD25^- T细胞分离后，对照组用CD3和CD28单抗活化，实验组在对照基础上加用卵巢癌细胞株SKOV3培养上清，72h后分离各组的CD25^＋和CD25^-T细胞，溴化脱氧尿嘧啶掺入标记法测定增殖能力及对静息的自体同源CD4^＋CD25^- T细胞的增殖抑制能力，流式细胞仪测定细胞糖皮质激素诱发型TNF受体（glucocorticoid-induced TNFR,GITR）与CTLA-4分子的表达，RT-PCR检测细胞卿mRNA的表达。结果与对照组相反，实验组的CD4^＋CD25^＋T细胞具有免疫抑制功能，自身增殖能力下降，GITR和CTLA-4分子的表达和CD4^＋CD25^＋调节性T细胞相似，并被诱导表达转录因子Foxp3 mRNA。结论卵巢癌细胞分泌的可溶性物质能诱导外周血CD4^＋CD25^-T细胞转化为CD4^＋CD25^＋调节性T细胞。     

Origin and T cell receptor diversity of Foxp3+CD4+CD25+ T cells

Foxp3(+)CD4(+)CD25(+) regulatory T cells can differentiate from Foxp3(-)CD4(+) medullary thymocytes and Foxp3(-)CD4(+) naive T cells. However, the impact of these two processes on size and composition of the peripheral repertoire of regulatory T cells is unclear. Here we followed the fate of individual Foxp3(+)CD4(+)CD25(+) thymocytes and T cells in vivo in T cell receptor (TCR) transgenic mice that express a restricted but polyclonal repertoire of TCRs. By utilizing high-throughput single-cell analysis, we showed that Foxp3(+)CD4(+) peripheral T cells were derived from thymic precursors that expressed a different TCRs than Foxp3(-)CD4(+) medullary thymocytes and Foxp3(-)CD4(+) T cells. Furthermore, the diversity of TCRs on Foxp3(+)CD4(+) regulatory T cells exceeded the diversity of TCRs on Foxp3(-)CD4(+) naive T cells, even in mice that lack expression of tissue-specific antigens. Our results imply that higher TCR diversity on Foxp3(+) regulatory T cells helps these cells to match the specificities of autoreactive and naive T cells.     

中国健康人外周血中具有CD4+CD25nt/hiCD127lo特征的调节性T细胞频率

目的：初步确定健康人外周血中具有CD4^＋ CD25^nt/hi CD127^lo特征的调节性T细胞（Treg）频率，为临床相关疾病的研究及Treg的分选提供参考。方法：采集312名8—60岁（5个年龄组）、不同性别健康人的静脉血，经三重免疫荧光染色，用流式细胞术分析CD4^＋ CD25^nt/hi CD127^lo Treg细胞频率，并观察细胞内Foxp3转录因子的表达。结果：健康人CD4^＋ CD25^nt/hi CD127^lo Treg细胞在外周血中约占CD4^＋ T细胞的（6．55±0．11）％，各年龄组之间有差异（P=0．015），组内性别之间也存在统计学意义（P〈0．05）； CD25^nt/hi CD127^lo细胞特异性地表达Foxp3转录因子。结论：初步确定了中国健康人外周血中具有CD4^＋ CD25^nt/hi CD127^lo表达特征的细胞频率，为Treg细胞的临床研究奠定了基础； CD25^nt/hi CD127^lo作为CD4^＋ CD25^＋ Treg细胞表面的特征性标志，可在分选时排除其他细胞干扰，获得较完整的Treg细胞。     

Dendritic cells partially abrogate the regulatory activity of CD4+CD25+ T cells present in the human peripheral blood

The factors that influence the functionality of human CD4(+)CD25(+) regulatory T cells are not well understood. We sought to characterize the effects of dendritic cells (DCs) on the in vitro regulatory activity of CD4(+)CD25(+) T cells obtained from peripheral blood of healthy human donors. Flow cytometry showed that a higher proportion of CD4(+)CD25(+(High)) T cells expressed surface glucocorticoid-induced tumor necrosis factor receptor family-related protein (GITR) and CTL-associated antigen 4 than CD4(+)CD25(-) or CD4(+)CD25(+(Med-low)) T cells. Intracellular Foxp3 was equivalently expressed on CD4(+)CD25(+(All)), CD4(+)CD25(+(High)), CD4(+)CD25(+(Med-low)) and CD4(+)CD25(-) T cell populations, irrespective of GITR and CTL-associated antigen 4 expression. CD4(+)CD25(+) T cells were isolated and then cultured in vitro with CD4(+)CD25(-) responder T cells and stimulated with anti-CD3 antibodies, and immature dendritic cells (iDCs), mature dendritic cells (mDCs), PBMCs or PBMCs plus anti-CD28 antibodies to provide co-stimulation. In addition, secretion of the T(h)1 cytokine IFN-gamma, IL-2 and the immunoregulatory cytokines, IL-10 and transforming growth factor (TGF)-beta, were also assessed in these cultures. We found that iDCs and mDCs were capable of reversing the suppression of proliferation mediated by CD4(+)CD25(+) regulatory T cells. However, the reversal of suppression by DCs was not dependent upon the increase of IFN-gamma and IL-2 production or inhibition of IL-10 and/or TGF-beta production. Therefore, DCs are able to reverse the suppressive effect of regulatory T cells independent of cytokine production. These results suggest for the first time that human DCs possess unique abilities which allow them to influence the functions of regulatory T cells in order to provide fine-tuning in the regulation of T cell responses.     

Reduction of forkhead box P3 levels in CD4+CD25high T cells in patients with new-onset systemic lupus erythematosus

The aim of this study was to quantify and evaluate the forkhead box P3 (FoxP3) expression regulatory T cells in new-onset systemic lupus erythematosus (SLE) patients before and after treatment. Forty-four newly diagnosed and untreated SLE patients, including 24 with active disease (SLEDAI > or = 10) and 20 with inactive disease (SLEDAI < 5), were enrolled in this study. Twenty-one age- and sex-matched healthy volunteers were also included as controls. Peripheral blood samples were collected and mononuclear cells isolated. The expression of CD25 and FoxP3 in CD4(+) T cells were analysed with flow cytometry. CD4(+)CD25(+) (3.95-13.04%) and CD4(+)CD25(high) (0.04-1.34%) T cells in peripheral blood in untreated patients with new-onset active lupus were significantly lower than that in the patients with inactive lupus (7.27-24.48%, P < 0.05 and 0.14-3.07% P < 0.01 respectively) and that in healthy controls (5.84-14.84%, P < 0.05). Interestingly, the decrease in CD4(+)CD25(high) T cells was restored significantly in patients with active lupus after corticosteroid treatment. There was, however, a significantly higher percentage of CD4(+)FoxP3(+) T cells in patients with active (5.30-23.00%) and inactive (7.46-17.38%) new-onset lupus patients compared with healthy control subjects (2.51-12.94%) (P < 0.01). Intriguingly, CD25 expression in CD4(+)FoxP3(+) T cells in patients with active lupus (25.24-62.47%) was significantly lower than that in those patients with inactive lupus (30.35-75.25%, P < 0.05) and healthy controls (54.83-86.38%, P < 0.01). Most strikingly, the levels of FoxP3 expression determined by mean fluorescence intensity in CD4(+)CD25(high) cells in patients with active SLE were significantly down-regulated compared with healthy subjects (130 +/- 22 versus 162 +/- 21, P = 0.012). CD4(+)CD25(high) T cells are low in new-onset patients with active SLE and restored after treatment. Despite that the percentage of CD4(+)FoxP3(+) T cells appear high, the levels of FoxP3 expression in CD4(+)CD25(high) T cells are down-regulated in untreated lupus patients. There is a disproportional expression between CD25(high) and FoxP3(+) in new-onset patients with active SLE.     

The role of CD4+CD25+ regulatory T cells in patients with Rheumatoid Arthritis]

CD4(+)CD25(+) regulatory T cells play an important role in preventing autoimmunity. We investigated the presence of CD4(+)CD25(+) regulatory T cells in the peripheral blood of patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and systemic sclerosis (SSc), using flow cytometry. The percentage of CD4(+)CD25(+) regulatory T cells was significantly decreased in RA, especially in patients with high serum levels of either CRP or MMP-3. In SSc and SLE, the percentage of CD4(+)CD25(+) regulatory T cells was higher in patients than in controls, but not significant. We also investigated the serum levels of IL-10, which influences the function of CD4(+)CD25(+) regulatory T cells and other regulatory T cells. In RA, on contrast to CD4(+)CD25(+) regulatory T cells, the serum levels of IL-10 increased in patients with higher serum levels of CRP, or MMP-3. In SLE and SSc, the serum level of IL-10 increased significantly in patients than in controls. These data thus indicated that CD4(+)CD25(+) regulatory T cells contributes to occurrence and progression of RA, and other regulatory T cells or cytokines contribute to occurrence and progression of SSc and SLE.     

新生儿脐带血CD4+CD25high调节性T细胞Foxp3的表达

目的:检测新生儿脐带血CD4 CD25high调节性T细胞(Treg)数量及胞内转录因子Foxp3的表达,探讨Treg细胞在新生儿期的表达特点.方法:采集新生儿脐带血(n=15)和成人外周血(n=12),密度梯度离心法获取单个核细胞用荧光标记单克隆抗体(mAb)作表面和胞内染色后,在流式细胞仪上检测CD4 CD25highTreg细胞的数量及其胞内转录因子Foxp3的表达.结果:脐带血Treg细胞占CD3 CD4 T细胞的比例(3.86%±1.63%)明显高于成人外周血(0.87%±0.74%,P<0.01);而脐带血Treg细胞中表达Foxp3的比例明显低于外周血Treg细胞(23.21%±8.9%vs71.3%±11.6%,P<0.01).结论:虽然新生儿脐带血CD4 CD25highTreg细胞数量明显高于成人外周血,但Foxp3 细胞数量明显低于成年人,提示在功能上可能尚未成熟.