依那西普治疗降低强直性脊柱炎外周血T细胞活性

目的 研究肿瘤坏死因子(TNF)-α抑制剂依那西普(Etanercepl)对强直性脊柱炎(AS)患者外周血T细胞活性的影响.方法 10例健康志愿者,40例活动性AS患者,随机给予依那西普(50 mg,皮下注射,每周1次)或安慰剂治疗,治疗前后分离外周血单个核细胞(PBMC),酶联免疫斑点法(ELISPOT)分别检测分泌TNF-α、白细胞介素(IL)-2、干扰素(IFN)-γ的细胞数量.WST-1法检测T细胞增殖.结果 依那西普治疗后,分泌TNF-α的单核细胞数量减少;抗CD3和抗CD28抗体刺激后,分泌IL-2和IFN-γ的T细胞数量减少.CD4+/CD8+T细胞增殖没有明显变化.结论 抗TNF-α的治疗降低了AS患者外周血T细胞的活性,改善了AS患者病情.     

老年高血压患者外周血T淋巴细胞表面抗原表达的研究

目的:探讨老年人外周血T淋巴细胞表面抗原CD45RA和CD45RO的表达及其与高血压的关系。方法:收集44例60岁以上老年人外周静脉血,按高血压诊断标准分为老年对照组(25例)和老年高血压组(19例),另收集20例健康成年人外周静脉血(成年对照组),均分离外周血单个核细胞,通过流式细胞仪检测CD45RA+和CD45RO+占CD4+T淋巴细胞的百分比,分析CD45RA和CD45RO抗原表达的相对关系。结果:老年对照组外周血CD45RA+占CD4+T淋巴细胞的百分比较成年对照组显著降低,CD45RO+占CD4+T淋巴细胞的百分比较成年对照组显著升高(均P0.05);与老年对照组相比,老年高血压组外周血CD45RO+占CD4+T淋巴细胞的百分比显著升高,45RA+/CD45RO+的比值显著降低(均P0.05)。结论:T淋巴细胞表面抗原CD45的表达变化提示T淋巴细胞的过度激活分化,可能参与了老年高血压的发病。     

系统性红斑狼疮患者外周血CD4+ CD8+和CD22+淋巴细胞活化分子CD69的表达

目的探讨系统性红斑狼疮(SLE)患者外周血淋巴细胞(PBL) T细胞(CD4+、CD8+)和B细胞(CD22+)活化分子CD69的表达.方法应用双染色流式细胞术检测CD4、CD8、和CD22细胞亚群CD69分子;在植物凝集素(PHA)刺激后20 h淋巴细胞亚群CD69分子的表达.结果①SLE患者PBMC的CD69分子活动期高于静止期(P＜0.001)和正常对照组(P＜0.01)的表达,SLE静止期患者与正常对照组CD69表达差异无显著性(P＞0.05).②进一步分析CD4+、CD8+和CD22+淋巴细胞亚群的CD69的表达,其中,SLE活动期患者CD4+细胞的CD69表达显著高于静止期(P＜0.001)和正常对照组(P＜0.01)的表达,SLE静止期患者与正常对照组CD69表达差异无显著性(P＞0.05);CD8+细胞活动期高于静止期患者(P＜0.05),其余组间差异无显著性(P＞0.05);CD22+B细胞各组间差异无显著性.③PHA刺激20 h后,CD4+、CD22+B细胞的CD69表达,活动期显著高于静止期患者和正常对照组(P＜0.01).结论 SLE患者外周血CD4+T细胞和CD22+B细胞存在着异常的活化,这种淋巴细胞的异常活化是SLE重要的发病机制之一.     

老年肺癌患者外周血T淋巴细胞亚群和自然杀伤细胞的临床及意义

目的探讨老年肺癌患者T淋巴细胞亚群和自然杀伤(NK)细胞水平及临床意义。方法该校附属医院80例老年肺癌患者作为观察组,回顾分析外周血T淋巴细胞亚群和NK细胞检测结果,与另选的80例健康受检者(对照组)进行对比分析,并于术后20 d复查肺癌患者的外周血T淋巴细胞亚群和NK细胞,对比缓解者与未缓解者的检查结果。结果外周血T淋巴细胞亚群与NK细胞表达水平检测中,观察组CD3+、CD4+、CD4+/CD8+比值与NK细胞水平较对照组明显降低(P0.05),CD8+表达水平明显高于对照组(P0.05)。观察组于术后20 d复查T细胞亚群和NK细胞,根据结果分为两组进行分析,发现缓解组CD3+、CD4+、CD4+/CD8+和NK表达均较化疗前明显上升,CD8+表达显著降低(P0.05)。而未缓解组各项指标化疗前后无明显变化(P0.05)。结论 NK细胞与外周血T淋巴亚群对诊断、评价肺癌的疗效、判断预后具有重要价值。     

类风湿关节炎患者外周血CD19+CD23+B淋巴细胞水平及其与疾病活动性的关系

目的 探讨类风湿关节炎(RA)患者外周血CD19+ CD23+B淋巴细胞检测水平与病情活动性的相关性.方法 选择RA患者50例(RA组)及健康体检者20例(对照组),分别采用流式细胞仪检测两组外周血CD19+ CD23+B淋巴细胞水平,分析其与RA患者疾病活动度的相关性.结果 RA组患者外周血CD19+、CD23+及CD23 +/CD19+细胞百分率均明显较正常对照组升高(P＜0.05).CD19+表达率与晨僵时间、关节压痛数、关节肿胀数、RF、PLT、DAS28呈正相关(均P＜0.05),而与ESR、C-反应蛋白无明显相关(均P＞0.05).CD23+及CD23 +/CD19+表达率与晨僵时间、关节压痛数、关节肿胀数、ESR、CRP、RF、PLT、DAS28呈显著正相关关系(均P＜0.05).结论 外周血中CD19+、CD23+及CD23+/CD19+淋巴细胞的异常表达在RA发病机制中可能起一定作用,且与疾病活动性相关.     

炎症性肠病患者T淋巴细胞亚群的改变及临床意义

目的探讨炎症性肠病(IBD)患者外周血T淋巴细胞亚群的变化特点及临床意义.方法对临床确诊的18例溃疡性结肠炎(UC)和9例Crohn病(CD)患者,于疾病的不同时期用荧光单克隆抗体标记-流式细胞仪技术检测其外周血T淋巴细胞亚群的变化,并结合临床和病理资料进行综合分析.结果UC患者缓解期时的CD3+、CD8+和自然杀伤(NK)细胞与对照组比较无显著差异;但活动期时,其CD8+和NK细胞数明显下降(CD8+活动期23.1%±1.0%,对照组31.3%±1.2%,P＜0.05;NK活动期9.8%±1.0%,对照组15.1%±1.1%,P＜0.01),CD4+/CDs+比值上升(活动期1.8±0.1,对照组1.4±0.02,P＜0.05);活动期CD患者的CD8+细胞和CD4+/CD8+比值(43.0%±44%和0.6±0.1)变化却与UC组活动期呈相反趋势(P＜0.01).结论T淋巴细胞亚群改变在IBD的发病机制中可能起重要作用;UC和CD的细胞免疫机制不同;外周血CD4+、CD8+、NK细胞和CD4+/CD8+比值可作为检测UC病情变化和疗效考核的敏感指标.     

慢性乙型肝炎患者外周血CD4+CD25+调节性T细胞和T淋巴细胞亚群的研究

目的 观察外周血CD4 CD25 调节性T细胞(Tregs)百分比和T淋巴细胞亚群在慢性乙型肝炎(CHB)患者中的特点.方法 采集CHB患者15例和健康对照20例的外周血单个核细胞(PBMC)标本,应用三色流式分析法对PBMC中CD4 CD25 Tregs占CD4 百分比及外周血中的T淋巴细胞亚群进行分析.结果 分别比较CD4 CD25highTregs和CD4 CD25 CD127low/-Tregs占CD4 T细胞百分比,两组表型的Tregs在CHB组均高于正常对照组[(4.25%±3.22%vs1.57%±0.64%),(4.39%±2.03%vs1.86%±0.84%)](P＜0.01).CHB组外周血中的CD4 T淋巴细胞亚群的百分比(32.28%±6.26%)较正常对照组(39.39%±10.73%)下降,统计学有差别(P＜0.05).外周血中CD8 及CD4 /CD8 比值在两组间变化无统计学差异.结论 CHB患者CD4 CD25high和CD4 CD25 CD127low/-Tregs升高,外周血中的CD4 T淋巴细胞百分比下降.     

慢性乙型肝炎患者外周血中淋巴细胞亚群与肝组织炎症活动度的相关性研究

目的 探讨慢性乙型肝炎患者外周血中淋巴细胞亚群与肝组织炎症活动度的关系.方法 对36例慢性乙型肝炎患者行肝脏穿刺术,对炎症程度进行病理分级,同时应用流式细胞技术测定其外周血单个核细胞膜上相关CD分子的表达情况,并与22例健康对照组进行比较分析.结果 15例G0～G2期患者外周血中CD4 CD45RO CD45RA-及CD8 CD45RA CD62L 淋巴细胞与健康对照组相比具有统计学差异(P<0.05);14例G3期患者外周血中CD3 、CD3 CD8 、CD8 CD28 、CD8 HLA-DR CD19 及CD3-CD19 淋巴细胞与健康对照组相比具有统计学差异(P<0.05);7例G4期患者外周血CD4 CD45RA CD62L 及CD19 CD5 淋巴细胞与健康组相比具有统计学差异(P<0.05);三组间淋巴细胞数均无统计学差异.不同组别的部分淋巴细胞之间具有一定的相关关系.结论 慢性乙型肝炎患者外周血中淋巴细胞亚群数量的改变与病情的轻重有一定的相关性;不同活动期的慢性乙型肝炎患者外周血淋巴细胞之间具有一定的相关关系.     

共刺激分子CD28 CD152在类风湿关节炎患者T细胞亚群上表达异常的研究

目的观察共刺激分子CD28,CD152在类风湿关节炎(RA)患者的T细胞亚群上的表达异常情况,探讨RA的发病机制及治疗手段.方法用流式细胞仪采用直接免疫荧光法测定39例RA患者和20名健康对照人外周血T细胞表面标志CD3,CD4,CD8的表达情况及CD28,CD152在CD4+T和CD8+T细胞上的表达.结果 RA患者CD3+CD4+细胞较正常对照组显著增高(P＜0.01),CD3+CD8+细胞较正常对照组显著降低(P＜0.05),CD4+T细胞上CD28的表达较对照组显著降低(P＜0.05),而CD8+T细胞上CD28的表达与对照组差异无显著性(P＞0.05);CD4+T和CD8+T细胞上CD152的表达都较对照组显著增高(P＜0.01).结论在RA患者的细胞免疫活化过程中首先表现为B7/CD28信号途径占优势,T细胞被激活,激活的T细胞大量分泌CD152,它与CD28竞争结合B7分子,CD152/B7途径转而占优势,下调或终止T细胞反应.同时CD28+细胞数目的减少或功能缺陷造成RA患者外周血单个核细胞凋亡加速,是诱发RA患者的局部病理损害的原因.阻断CD152和B7的相互作用可增强特异性T细胞应答,为RA的免疫学治疗提供理论依据.     

原发性肝癌和乙型肝炎肝硬化患者外周血淋巴细胞凋亡率、T细胞亚群和NK细胞的水平变化和临床意义

目的通过检测乙型肝炎肝硬化和合并乙型肝炎病毒感染的原发性肝细胞癌患者的外周血的粒细胞、单核细胞、NK细胞、T细胞及其亚群和淋巴细胞及其凋亡率,探讨两者在细胞免疫方面的差异.方法用Ficoll Hypaque离心法分离外周血单个核细胞(PBMNC),流式细胞仪检测外周血T细胞及其亚群、NK细胞和淋巴细胞、单核细胞和粒细胞,AnnexinV/FITCKit检测凋亡细胞.结果乙型肝炎肝硬化患者的外周血单核细胞、粒细胞、淋巴细胞、CD3-CD16 CD56 NK细胞、CD3 T细胞、CD3 CD4 T细胞、CD3 CD4 T细胞和CD4 CD8 T细胞比值,均与正常对照组无显著性差异(P＞0.05);但淋巴细胞凋亡率明显低于对照组(P＜0.01).原发性肝癌外周血CD3-CD16 CD56 NK细胞、单核细胞和CD4 /CD8 T细胞比值与肝硬化组和正常对照组比较,均无显著性差异(P＞0.05),而粒细胞明显升高(P＜0.05);CD3 T细胞、CD3 CD4 T细胞和CD3 CD8 T细胞均较另两组明显减少(P＜0.05),淋巴细胞及其凋亡率均明显低于另两组(P＜0.01).结论乙型肝炎肝硬化患者的外周血细胞免疫只发生不显著的变化,但淋巴细胞的凋亡率明显降低.原发性肝癌外周血的细胞免疫和淋巴细胞凋亡率均明显低下.     

Abnormal high-expression of CD154 on T lymphocytes of ankylosing spondylitis patients is down-regulated by etanercept treatment

The pathogenesis of ankylosing spondylitis (AS) still remains an enigma. Although some studies have indicated the importance of T-cells and proinflammatory cytokines in the pathogenesis of the AS, it is still unknown whether co-stimulatory molecule CD154 participates in the pathogenesis of AS and how its level changes during the anti-TNF-α treatment of AS. This study is performed to evaluate the expression of CD154 in peripheral blood T-lymphocytes of patients with AS and observe the change of CD154 in etanercept-treated AS patient. We collected the peripheral blood and clinical data from 66 AS, 30 rheumatoid arthritis (RA) patients, and 30 healthy controls. Thirty-nine active AS patients were enrolled in a randomized double-blind placebo-controlled trial. We followed up 37 cases that fulfilled the ASAS20 response criteria after they finished etanercept treatment till week 48. The percentage of CD3+CD154+ in peripheral blood lymphocytes was evaluated by flow cytometry. We found that CD154 expression in AS patients was significantly higher than that in healthy volunteers and RA patients (both P < 0.001). The expressions of CD154 in AS patients at active stage or with peripheral joint involvement were significantly higher than those at stable stage or with axial involvement alone (P = 0.005 and 0.044, respectively). The expression of CD154 decreased in AS patients treated with etanercept compared with patients treated with placebo at week 6 (P < 0.001). Compared with healthy volunteers, the expression of CD154 in 16 AS patients who relapsed after finishing etanercept treatment was elevated again (P = 0.012). These findings show that co-stimulatory molecule CD154 is overexpressed on T-lymphocytes in peripheral blood of AS patients and can be down-regulated by etanercept treatment, which suggest that CD154 might be involved in the inflammatory evolvement of AS and might be a potential biomarker to monitor AS disease activity and the effect of etanercept treatment.     

强直性脊柱炎患者外周血CD4+CD25+调节性T细胞的研究

目的 观察强直性脊柱炎(AS)患者外周血CD4+CD25调节性T细胞(Treg)的数量、功能及肿瘤坏死因子(TNF)-a 抑制剂治疗的影响.方法 活动性AS患者25例,10例给予etanercept治疗12周,健康对照21名,分离外周血单个核细胞(PBMC),流式细胞术检测CD4+CD25high T细胞比例;实时定量聚合酶链反应检测FOXP3 mRNA表达;免疫磁珠法去除CD25+细胞,可溶性噻唑盐(WST-1)法检测T细胞增殖.结果 活动性AS组CD4+CD25high T细胞比例与对照组差异尤统计学意义,但FOXP3 mRNA表达明显低于对照组(P＜0.01),并与C反应蛋白(CRP)呈负相关(P＜0.01).两组的CD4+CD25+细胞体外均能抑制T细胞增殖(P均＜0.01). Etanercept治疗明显增加CD4+CD25highT细胞比例和FOXP3 mRNA表达(P均＜0.01),与CRP降低呈负相关(P＜0.05;P＜0.01).结论 AS患者外周血表达FOXP3的CD4+CD25+Treg细胞异常,可能参与AS发生和发展;Etanercept治疗上调Treg细胞,可能是抗TNF-α治疗的一个机制.     

慢性肾炎患者外周血共刺激分子CD28和CD137水平变化研究

目的　研究慢性肾炎患者外周血共刺激分子CD2 8和CD1 37的表达特点及其在慢性肾炎免疫病理机制中的作用。方法　采用免疫荧光标记和流式细胞仪分析 ,对 5 2例慢性肾炎患者外周血共刺激分子CD2 8、CD1 37和T淋巴细胞亚群的表达进行检测。结果　慢性肾炎患者T细胞亚群明显失衡 ,表现为CD4减少 ,CD8增加 ,CD4 CD8比值显著降低。共刺激分子CD2 8表达显著低于正常对照组 (P <0 0 1) ,且CD+4 CD+2 8T细胞和CD+8CD+2 8T细胞均显著减少 (P <0 0 1)。共刺激分子CD1 37表达显著高于正常对照组 (P <0 0 1)。结论　慢性肾炎患者外周血T细胞亚群失衡和T细胞活化所必需的共刺激分子CD2 8、CD1 37异常表达 ,可能在慢性肾炎发生和病变进展中起着重要作用     

Lymphocyte subsets of the peripheral blood in Sj?gren's syndrome and rheumatoid arthritis

Lymphocyte subsets were determined in the peripheral blood from twenty-three patients with primary Sj?gren's syndrome (SS) and sixteen patients with clinically active rheumatoid arthritis (RA) by two-color flowcytometry using various monoclonal antibodies. In both diseases, T-cells (CD3+), suppressor/cytotoxic cells (CD8+) and their cytotoxic subset (CD8+CD11-) were decreased, as compared with thirty-one healthy controls. B-cells (CD 21+ and CD 3-DR+) and activated T-cells (CD 3+DR+) were increased in SS patients. Helper T-cells (CD 4+Leu8-), suppressor-inducer T-cells (CD4+Leu8+), suppressor T-cells (CD8+Leu 15+) and three natural killer (NK) cell subsets determined by both CD16 and Leu7 antibodies did not differ between controls and SS or RA, although Leu7+NK cells were significantly increased in SS patients. In addition, we found that the treatment with low-dose prednisolone decreased B-cells and suppressor-inducer T cells, and increased suppressor T-cells, cytotoxic T-cells and Leu7+NK cells. The results indicate similar changes in the proportion of lymphocyte subsets and suggest immunologically activated and deficient conditions in both diseases. Immunomodulating effects of the treatment with low-dose prednisolone on some of the lymphocyte subsets in patients with these diseases were also supported by the study.     

Cd28 expression on t cell subsets in vivo and cd28-mediated t cell response in vitro in patients with rheumatoid arthritis

Objective. In view of the critical importance of the CD28–CD80 (B7/BB1) costimulatory pathway in antigen-specific T cell activation and clonal expansion, we examined CD28 surface molecule expression in vivo, and T cell receptor/CD3-mediated and B7/BB1-costimulated T cell proliferation in vitro, in rheumatoid arthritis (RA). Methods. Two-color immunofluorescence analyses of peripheral blood and synovial fluid–derived T cells, as well as ³H-thymidine incorporation assays, were performed. Results. In the peripheral blood of 31 patients with active, untreated RA, a mean of 91% (range 48–100%) of CD4+ and 46% (range 13–82%) of CD8+ T cell subsets were CD28+, which was not significantly lower than normal. Although an overall decrease in the number of T cells was not observed, the numbers of CD28+CD8+ T cells were significantly lower in RA patients (mean 233/μl, versus 292/μl in controls), and this decrease was more pronounced in patients with severe disease (mean 172/μl). CD28 expression on peripheral CD8+ T cells in RA patients, but not in healthy individuals, correlated inversely with T cell activation as assessed by HLA–DR antigen expression. In contrast to the peripheral blood, RA synovial fluid T cells were almost exclusively CD28+, suggesting that migration of CD28+CD8+ T cells to active sites of inflammation may occur. In vitro proliferative responses of peripheral blood T cells to B7/BB1 costimulation in the presence of mitogenic doses of anti-CD3 monoclonal antibody were identical in patients with RA and healthy individuals. Conclusion. Functionally intact CD28+ T cells may contribute to the abnormal immunoregulation and joint inflammation in RA.     

Comparison of blood and synovial fluid lymphocyte subsets in rheumatoid arthritis and osteoarthritis

Summary Immunoregulatory T-cell deficiency is thought to underlie pathogenesis of rheumatoid arthritis (RA) as a systemic autoimmunopathy. The aim of this study was a simultaneous analysis of peripheral blood and synovial lymphocyte subsets (Ly-SS) of RA patients as compared to patients with locally active osteoarthritis (OA). Peripheral blood Ly-SS and paired synovial fluid Ly-SS from 87 RA patients were analysed by two dimensional flow cytometry (Simulset Becton Dickinson) as compared to 15 OA patients. The control group consisted of 32 healthy subjects. The peripheral blood analysis from RA and OA patients revealed a significant decrease of CD8+T-cells and increase of CD4+:CD8+ ratio when compared to the control group. The blood of RA patients showed a significant increase of HLA DR+ and IL 2R+T cells as compared to OA group. The synovial fluid from RA and OA patients showed a significant increase of CD3+, CD8+, HLA DR+ T-cells and decrease of CD4+:CD8+ ratio and CD19+ cells in comparison to the peripheral blood. This study shows, that the OA T-cell system seems not to be activated in peripheral blood in opposition to RA patients. Synovial fluid Ly-SS in OA, however, showed only quantitative but not qualitative differences. OA seems to be mainly a local inflammatory response depending on T-cells, when lymphocyte T activity in blood is diminished.     

强直性脊柱炎患者外周血CD8+CD28-T细胞的表达及意义

目的 探讨外周血CD8+CD28- T细胞在强直性脊柱炎(AS)发病中的作用.方法 应用流式细胞术检测50例AS患者和21名正常人外周血CD3+CD8+ T细胞表面CD28分子的表达,同时用免疫散射比浊法检测相应血清中的C反应蛋白(CRP).结果 AS患者外周血中的CD8+CD28- T细胞的表达明显高于正常人[(18±6)%对(14±5)%,P=0.020],患者外周血CD3+、CD8+CD28+ T细胞的表达明显低于正常人[(65±9)%对(69±8)%,P=0.039];[(15±5)%对(18±4)%,P=0.038],CD8+ T细胞的表达与正常人相比差异无统计学意义(P＞0.05).结论 AS患者外周血中的CD8+CD28- T细胞的表达增加,可能参与了AS的疾病过程.     

Increased expression of CD154 (CD40L) on stimulated T-cells from patients with psoriatic arthritis

OBJECTIVES: CD40L is a costimulatory molecule and an early activation marker of T-lymphocytes. Based on the hypothesis that activated T-cells may play a role in the pathogenesis of psoriatic arthritis (PsA), we evaluated the level of CD40L expression on T-cells from patients with PsA. METHODS: We analysed 12 patients with PsA, six patients with rheumatoid arthritis (RA) and four healthy volunteers. T-cell surface expression of CD40L was evaluated using two-colour flow cytometry in (i) the resting state and (ii) following stimulation with phorbol myristate acetate/ionomycin, with or without ciclosporin (CsA)-mediated inhibition. RESULTS: Expression of CD40L was significantly increased on activated T-cells from patients with PsA, particularly those with active disease, when compared with normal individuals and patients with RA (mean percentages of CD3+ CD40L+ cells: 23.74, 11.59 and 9.57% for patients with active PsA, patients with RA and healthy volunteers, respectively). CsA-mediated inhibition of CD40L induction was equally effective in all study groups. CONCLUSION: CD40L is overexpressed on T-cells from patients with active PsA. This may indicate a role for CD40L in PsA pathogenesis. Larger-scale studies are warranted to address these issues.     

Mechanisms of CD23 hyperexpression on B cells from patients with rheumatoid arthritis.

OBJECTIVE: To analyze the mechanisms involved in the characteristic hyperexpression of CD23 on peripheral blood B cells from patients with rheumatoid arthritis (RA). METHODS: Peripheral blood mononuclear cells (PBMC) were obtained from patients with active disease and activated during 18 h with an anti-CD3 monoclonal antibody in the presence or absence of blocking antibodies to CD154 or CD40. PBMC were further purified by rosetting and CD23 expression was assessed on B cells by flow cytometry after double staining (CD19/CD23). Lymphocytes were also isolated from synovial fluid (SF). CD154 expression was analyzed on PB or SF CD4+ T cells after double staining (CD4/CD154) by flow cytometry at basal conditions and after different stimuli [anti-CD3 or phorbol myristic acetate (PMA) plus ionomycin]. Co-culture experiments between SF and PB cells were performed to analyze the involvement of the CD40-CD154 interaction on CD23 expression. CD154 and CD23 expression was also analyzed on synovial membrane by immunohistochemical techniques. RESULTS: A high proportion of activated CD23 B cells was detected in patients with RA. Blocking experiments with both anti-CD40 and anti-CD154 Mab showed a significant reduction in the proportion of PB B cells expressing CD23. Following activation with anti-CD3 Mab or PMA plus ionomycin, CD154 expression was mainly induced on PB CD4+ T cells. In co-culture experiments, SF T cells were more efficient than PB T cells in inducing CD40 dependent CD23 expression on PB B cells. In addition, CD4+ T cells from synovial membrane clearly expressed CD154. CONCLUSION: Our results establish a link between CD154-CD40 pathway and CD23 expression on PB B cells from patients with RA. T cells from the synovial microenvironment were active participants in this CD23 expression, presumably in the context of cell recirculation.     

Resting and Activated Natural Tregs Decrease in the Peripheral Blood of Patients with Atherosclerosis

Background: Atherosclerosis is a chronic inflammatory disease affecting large and medium arteries. CD4+ T cells are known to play a role in the progression of the disease. CD4+CD25+Foxp3+ natural Treg (nTreg) cells seem to have a protective role in the disease and their reduction in acute coronary syndrome is recently shown. Objective: To investigate the frequency of nTreg subsets in the peripheral blood of patients with atherosclerosis. Methods: Confirmation of atherosclerosis was done by angiography and 15 ml heparinized blood was obtained from each of the 13 nondiabetic patients and 13 non-diabetic, non-smoker individuals with normal/insignificant coronary artery disease which was also confirmed by angiography. Lipid profiles of the patients and controls were measured at the time of sampling. Mononuclear cells were used for both RNA extraction and immunophenotyping by real-time PCR and flowcytometry techniques, respectively. Results: In natural Treg subsets, the frequency of CD4+CD45RO-CD25+Foxp3lo T-cells (resting nTregs) was greater in controls than patients (p=0.02). The frequency of CD4+CD45RO+CD25hiFoxp3hi T-cells (activated nTregs) was significantly higher in controls compared with patients (p=0.02). However, the frequency of CD4+CD25+CD45RO+Foxp3- T-cells (effector/memory) increased in patients compared with controls (p=0.01). Both the MFI and gene expression of Foxp3 were higher in control group than in patients (p=0.015 and p=0.017, respectively). Moreover, the TGF-β gene expression showed a decrease in the peripheral blood mononuclear cells of patients compared with controls (p=0.03). Conclusion: Decrease in both subsets of resting and activated nTregs along with a decrease in the expression of Foxp3 and TGF-β genes in patients with atherosclerosis suggests phenotypic changes in these subsets, which may as well be correlated with a more inflammatory profile in their lymphocytes.