老年大鼠T细胞凋亡相关基因表达模式的研究

目的　探讨老年大鼠 T细胞凋亡的基因表达模式。方法　本研究利用 TUNEL标记的流式细胞检测和荧光实时定量 RT- PCR技术 ,研究了老年大鼠和年轻大鼠 T淋巴细胞凋亡情况及抗凋亡和促凋亡基因 (Fas,Fas L ,bcl- 2 ,bax,TNFR1 ,TNFR2 )的表达差异 ,以及 Caspase8、Caspase3活性的变化。结果　与年轻大鼠相比 ,老年大鼠激活诱导的细胞凋亡百分率增高 ,有显著性差异 (P<0 .0 1 ) ;老年大鼠促凋亡的 Fas,Fas L,TNFR1基因表达上调 ,抗凋亡的 bcl- 2 ,TNFR2基因表达下调 ,与年轻大鼠相比均有显著性差异 (P<0 .0 5或 P<0 .0 1 )。此外 ,老年大鼠激活诱导的T淋巴细胞 Caspase8、3活性增高 ,与年轻大鼠相比有显著性差异 (P<0 .0 1 )。结论　激活诱导的 T细胞过度凋亡与衰老密切相关 ;促凋亡基因表达上调及抗凋亡基因表达下调及 Caspase8、3活性增高是老年大鼠 T细胞凋亡易感性增高重要分子机制。     

益气除痰方对大鼠肺癌A549细胞的抑制作用及其机制

目的探讨益气除痰方对肺癌A549细胞的抑制作用及与细胞凋亡相关的机制。方法以四甲基偶氮唑蓝(MTT)比色法和流式细胞术碘化丙啶(PI)单染法检测益气除痰方对肺癌A549细胞活力和细胞凋亡率的影响,RT-PCR方法检测p53、bcl-2和bax的m RNA表达水平。结果MTT法检测结果表明益气除痰方显著抑制A549细胞的生长(P<0.05或P<0.01),抑制作用随药物作用时间和浓度增大而增大;流式细胞术结果表明益气除痰方对A549细胞的凋亡诱导作用随着药物剂量的增加而显著增大(P<0.05);RT-PCR结果显示与对照组(p53基因1.58±0.91、bax基因3.27±1.55和bcl-2基因12.09±2.67)相比,益气除痰方引起p53和bax的m RNA表达显著上调(p53和bax分别为13.89±2.52和12.83±1.95,P均<0.01),但bcl-2的m RNA表达显著下调(9.86±2.12,P<0.05)。结论益气除痰方可诱导肺癌A549细胞凋亡,具有抑制其生长的作用,这可能与p53和bax表达上调、bcl-2表达下调有关。     

硝酸甘油对心肌细胞凋亡和Fas基因蛋白及mRNA表达的影响

目的　探讨硝酸甘油对持续缺血和缺血再灌注损伤时心肌细胞凋亡和 Fas基因蛋白及 m RNA表达的影响。方法　将大白鼠随机分为 5组 ,以活结结扎左冠状动脉的前降支 ,分别造成阻断冠脉血流和再灌注。以缺口末端标记法 (TUNEL)标记凋亡细胞 ;以 S- P免疫组化及逆转录聚合酶链反应 (RT- PCR)法分别检测 Fas基因蛋白与 m RNA的表达变化。结果　凋亡细胞原位标记与半定量分析表明 :硝酸甘油处理组与持续缺血组、缺血再灌注组比较心肌细胞凋亡程度明显降低 ,Fas基因蛋白及 m RNA表达明显减少。结论　硝酸甘油预处理能能明显减轻心肌细胞凋亡程度 ;其机制可能与下调 Fas基因蛋白及 m RNA表达有关。     

急性白血病细胞体外对Jurkat细胞凋亡的影响

为探讨白血病细胞凋亡相关基因 (Fas)的功能性表达情况 ,将 2 7例白血病患者的白血病细胞与 Jurkat细胞体外孵育后 ,用原位末端标记法 (TUNEL )测定单纯 Jurkat细胞 (对照组 )、不加和加入不同浓度抗凋亡相关基因配体 (Fas L)的 Jurkat细胞凋亡率。结果显示 ,不加抗 Fas L 急性非淋巴细胞白血病组 (ANL L 组 )与对照组比较 ,凋亡率明显增高 (P<0 .0 1) ,急性淋巴细胞白血病组 (AL L 组 )与对照组比较仅轻度增高 (P<0 .0 5 ) ,两者均随细胞浓度的增加而凋亡率增高 ;ANL L组加与不加抗 Fas L 相比凋亡率明显减少 (P<0 .0 1) ,随抗 Fas L浓度的增加而凋亡率减少 ,AL L 组加与不加抗 Fas L 相比凋亡率轻度减少 (P<0 .0 5 ) ,也随抗 Fas L 浓度的增高而减少 ,但不如 ANL L组凋亡率变化明显。提示急性白血病细胞存在 Fas L的功能性表达 ,ANL L较 AL L的 Fas L表达高     

脑尔康对Alzheimer病小鼠脑细胞凋亡相关基因表达的影响

目的　观察复方中药脑尔康对 Alzheimer病 (AD)模型小鼠 ,学习记忆障碍的改善作用及对凋亡相关基因的调控作用。方法　用跳台法测试各组小鼠学习记忆功能 ,用 SP免疫组化法检测 Fas、Bcl- 2阳性细胞计数。结果　模型组与空白对照组比较 ,触电时间延长 ,潜伏期缩短 ,错误次数增多 ;Fas、Bcl- 2表达升高 (均 P<0 .0 1 )。各用药组与模型组比较触电时间缩短 ,潜伏期延长 (均 P<0 .0 5) ,Fas、Bcl- 2表达下调 (P<0 .0 5或 P<0 .0 1 )。各参数中药中、小剂量组优于西药组。结论　脑尔康能改善 AD小鼠学习记忆障碍具有促智作用 ,可通过调控凋亡相关基因表达 ,抗脑细胞凋亡 ,减少神经元丢失 ,而发挥抗痴呆作用     

沉默Survivin人耐药肺癌细胞凋亡相关基因表达变化及临床意义

目的探讨沉默Survivin基因后人耐药肺腺癌(A549DDP)细胞系凋亡相关基因表达变化及临床意义。方法应用RT-PCR法及Western印迹法比较Survivin在人肺腺癌A549细胞系及其耐药A549DDP细胞系的表达水平;通过小分子RNA干扰沉默Survivin基因,并采用微阵列PCR基因芯片(PCR-Array)技术比较沉默Survivin后A549DDP细胞凋亡相关基因表达水平变化。结果 (1)Survivin mRNA、Survivin蛋白在人耐药非小细胞肺癌细胞系呈现高表达。(2)沉默Survivin后A549DDP细胞部分抗/促凋亡基因表达发生改变,促凋亡基因TP53、CASP3、CASP7呈高表达,抗凋亡基因bcl-2、TRAF1、BFAR呈低表达。结论 (1)Survivin与部分抗/促凋亡基因共同参与了非小细胞肺癌耐药的发生。(2)封闭Survivin可改变耐药肺癌细胞的促/抗凋亡基因的表达,Survivin可能作为上游调控点参与调控部分促/抗凋亡基因组的表达。(3)Survivin可能成为逆转肺癌耐药的一个新靶点。     

Fas转导大肠癌细胞中凋亡相关基因表达的变化

目的观察Fas转导大肠癌细胞株在诱导细胞凋亡中凋亡相关基因的变化,进一步探讨凋亡信号传导途径。方法运用流式细胞直接免疫荧光术(FICM)检测凋亡相关基因的表达。细胞分组包括:Fas转导细胞组(对照组)、Fas转导细胞+Fas抗体组(12 h)、Fas转导细胞+Fas抗体组(24 h),Fas抗体浓度1∶100。结果在Fas抗体诱导的Fas转导株大肠癌细胞凋亡中,bcl-2蛋白表达水平明显下降(P0.01);bax蛋白表达水平有所增加(P0.05)。初步验证了Fas途径诱导的细胞凋亡中部分凋亡相关基因变化。结论Fas表达大肠癌细胞株在Fas抗体作用下能够有效通过下调bcl-2及上调bax表达诱导细胞凋亡。     

日本血吸虫感染过程中宿主CD^＋4CD^＋8T细胞凋亡的相关基因转录水平的研究

目的：探讨在日本血吸虫感染的过程中,宿主CD^ 4和CD^ 8T细胞凋亡的相关基因p53,bcl-2,TGFβ在转录水平上的变化,方法：用地高辛标记的探针作原位杂交,观察凋亡相关基因在日本血吸虫感染过程中CD ^ 4和CD^ 8T细胞中转录水平的变化,结果：在日本血吸虫感染过程中,CD^ 4和CD^ 8T细胞中促凋亡基因p53和TGF－βRNA的表达随感染时间的延长而升高,感染后第10周起CD^ 4T 细胞p53和TGF－βmRNA的表达明显高于CD^ 8T细胞,差异有显著意义,抑制凋亡发生的基因bcl-2mRNA表达水平则与之相反,CD^ 4T细胞bcl-2mRNA的表达从感染从第10周起显著下降,而CD^ 4T细胞bcl-2mRNA的表达水平无显著性变化,结论：在日本血吸虫感染过程中,CD^ 4T细胞凋亡比率超过CD^ 4/CD^ 8T细胞,CD^ 4/CD^ 8T细胞比值下降与p53,bcl-2,TGF-β基因的活化有关。     

依那普利、洛沙坦合用对自发性高血压病鼠心肌细胞bcl-2、Fas蛋白表达的影响

分别用依那普利(依那普利组)、洛沙坦(洛沙坦组)及两者合用(合用组)喂养28只自发性高血压病大鼠(SHR).不喂养任何药物的SHR作为空白对照组.另择Wistar-Kyoto鼠作为对照组.采用免疫组化S-P法检测各组Fas、bcl-2的表达.结果与对照组比较,空白对照组、依那普利组、洛沙坦组Fas升高、bcl-2降低;与空白对照组比较,依那普利组、洛沙坦组及合用药组Fas降低、bcl-2升高.以合用药组为著(P＜0.05,＜0.01).提示,依那普利组、洛沙坦合用较单独用药能更有效地调节SHR心肌细胞的抗凋亡基因与促凋亡基因表达失衡,减少细胞凋亡.     

黄芪多糖对H_2O_2所致乳鼠心肌细胞凋亡的影响

目的研究黄芪多糖(APS)对H_2O_2所致乳鼠心肌细胞凋亡的影响,并探讨其可能的作用机制。方法分离并培养乳鼠心肌细胞72 h后分为:空白对照组、H_2O_2组、APS(20μmol/L、40μmol/L和80μmol/L)+H_2O_2组,每组设10个复孔;给药干预24 h后,MTT法检测细胞存活率,通过流式细胞术(Flow Cytometry)检测细胞凋亡状况并计算凋亡率;测定细胞中抗氧化酶[超氧化物歧化酶(SOD)、过氧化氢酶(CAT)]活性和丙二醛(MDA)含量,培养液中心肌酶[谷草转氨酶(AST)、磷酸肌酸激酶(CPK)、乳酸脱氢酶(LDH)]含量,Western blot法检测细胞中NF-κB、caspase-3蛋白表达并进行半定量分析,RT-PCR法检测AKT m RNA、bcl-2 m RNA、Bax m RNA表达并计算bcl-2/Bax表达比值。结果与H_2O_2组比较,APS(40μmol/L、80μmol/L)+H_2O_2组细胞存活率显著升高,细胞凋亡率显著降低;细胞中SOD、CAT活性显著升高且MDA含量显著降低,培养液中AST、CPK、LDH含量显著降低,细胞中caspase-3、NF-κB蛋白表达量显著降低,AKT m RNA和bcl-2 m RNA表达显著上调,Bax m RNA表达显著下调,bcl-2/Bax表达比值显著升高,差异均有统计学意义(P0.05或P0.01)。结论 APS可能通过改善抗氧化酶活性、降低氧化应激损伤、降低NF-κB、caspase-3蛋白表达、上调抗凋亡基因表达并下调促凋亡基因表达、提高bcl-2/Bax表达比值,从而对H_2O_2诱导乳鼠心肌细胞凋亡起抑制作用。     

补肾煎对去势高脂血症兔ox-LDL及ox-LDL mRNA表达作用的实验研究

目的　观察补肾煎对去势高脂血症兔血 ox- LDL水平以及内皮细胞 ox- L DL m RNA表达的影响。方法　纯种新西兰雌兔去势术 +0 .5%胆固醇饲料 +静注牛血清白蛋白造模 ,模型动物连续使用雌激素和补肾煎治疗 1 2 w后检测相关指标。结果　与模型组相比 ,补肾煎较好地降低 ox- L DL含量 (P<0 .0 5) ,减少内皮细胞 ox- LDL m RNA的表达 (P<0 .0 5)。结论　补肾煎可改善去势高脂血症模型兔异常的血 ox- LDL水平 ,减少内皮细胞 ox- L DL m RNA的表达 ,从而减少 LDL氧化修饰 ,保护内皮细胞功能、防治绝经后动脉粥样硬化。     

哮喘患者外周血T淋巴细胞凋亡及其分子机制

目的　探讨哮喘患者外周血 Ｔ淋巴细胞凋亡率的变化及其分子机制。方法　取１２ 例急性发作期哮喘患者（ 哮喘组） 及１０ 名正常对照者（ 对照组） 外周血淋巴细胞并无菌分离 Ｔ 淋巴细胞,采用电镜和原位末端终止法（ Ｔ Ｕ Ｎ Ｅ Ｌ） 观察抗 Ｃ Ｄ＋３ 单抗（１００ ｍｇ／ Ｌ） 诱导体外培养０ 、２４ 、４８ 、７２ 小时后 Ｔ淋巴细胞凋亡变化,同时采用细胞原位杂交法观察不同培养时间 Ｔ 淋巴细胞 Ｂｃｌ２ ｍ Ｒ Ｎ Ａ 及 Ｂａｘｍ Ｒ Ｎ Ａ表达变化。结果　正常组及哮喘组 Ｔ 淋巴细胞抗 Ｃ Ｄ＋３ 单抗诱导后均出现凋亡典型形态改变,哮喘患者外周血 Ｔ细胞经抗 Ｃ Ｄ＋３ 单抗诱导２４ 小时后凋亡率为（９１９ ±２２５） ％ ,４８ 小时为（１５８９ ±２１８） ％ ,７２ 小时为（２１３７ ±３２４） ％ ;与正常组２４ 小时（１７９ ±２２２） ％ 、４８ 小时（２５２５ ±３５３） ％ 、７２ 小时（３５１４ ±２５３） ％ 比较,差异有显著性（ Ｐ 均＜ ００１） ,哮喘组７２ 小时方接近正常组２４ 小时水平。哮喘组 Ｔ 淋巴细胞凋亡抑制基因 Ｂｃｌ２ ｍ Ｒ Ｎ Ａ 的表达各时相均与正常组比较,差异有显著性（ Ｐ＜ ００１） 。而凋亡促进基因     

Age-related impairment of p56lck and ZAP-70 activities in human T lymphocytes activated through the TcR/CD3 complex.

Cellular immune responses decrease with aging. Lymphocytes of aged individuals do not perform as well as cells from young subjects in a number of in vitro assays including cell proliferation, cytokine production, and protection against apoptosis. Here, we have tested the hypothesis that a decrease in T cell responses in tymphocytes from elderly subjects could parallel a decrease in the activity of protein tyrosine kinases (PTK) associated with signal transduction in T lymphocytes. We report that anti-CD3-triggered T lymphocyte proliferation was significantly decreased in T lymphocytes from elderly subjects, but the decrease was not due to an alteration of the percentage or mean fluorescence intensities of CD3, CD4, and CD45. Of significance, the activities of p56lck and ZAP-70 in vitro were significantly decreased in T lymphocytes from elderly subjects compared to young individuals. However, the level of expression of the two kinases did not change with aging. The activity of p59fyn did not show changes with aging, suggesting that p59fyn did not compensate for the decreased activity of p56lck. We also found that the extent of tyrosine phosphorylation of the adaptor protein p95vav was similar in activated T lymphocytes from elderly and young subjects. Our results suggest that the altered cellular immune responses observed in T lymphocytes with aging may be the result, at least in part, of an alteration in early events associated with signal transduction through the TcR/CD3 complex that translates into decreased activities of p56lck and ZAP-70. Impairment in the activities of these twokey components of T cell signaling may contribute to reduced immune functions associated with aging.     

Medication non-adherence and poor glycaemic control in patients with type 2 diabetes mellitus

AimsHyperglycemia causes generation of free radicals which leads to oxidative stress and apoptosis in various cells. The present study was undertaken to investigate the correlation between oxidative stress and apoptotic markers in lymphocytes of diabetic patients with chronic non healing wounds.MethodsThirty healthy, thirty uncontrolled type 2 diabetes mellitus (T2DM) and thirty uncontrolled T2DM with chronic, non healing, neuropathic diabetic foot patients were included in this study. Indices of oxidative stress inside the lymphocyte lysate were estimated by measuring content of superoxide dismutase (SOD), Catalase, Glutathione and malonaldialdehyde (MDA). Protein expression studies of pro and anti apoptotic markers were carried out to elucidate their possible involvement in diabetic context.ResultsSOD and MDA activity was significantly higher in the lymphocytes of diabetic patients having chronic, non healing diabetic wound as compared with healthy (p < 0.001); whereas catalase and GSH activity was significantly reduced (p < 0.001) in the same group. Expressions of pro apoptotic markers (Caspase-3, Fas and Bax) were significantly higher whereas reduced expression of anti-apoptotic marker (Bcl-2) were obtained in lymphocytes of diabetic and non diabetic individuals.ConclusionsHyperglycemia confers pro apoptotic manifestations which are mostly through altered indices of oxidative stress within lymphocytic milieu.     

过敏性紫癜急性期患儿淋巴细胞凋亡特征的研究

为探讨过敏性紫癜(HSP)患儿急性期外周血淋巴细胞凋亡特征及其与T淋巴细胞免疫应答活性的相关性，选择HSP患儿及健康儿童各33例(HSP组及对照组)，分别应用形态法、间接免疫荧光法检测外周血淋巴细胞凋亡率、T淋巴细胞亚群及CD^ 23细胞百分率。结果HSP组急性期外周血淋巴细胞培养前及培养、48小时凋亡率均显著高于对照组(P均＜O．01)，外周血CD^ 4细胞百分率及CD^ 4／CD^ 4均明显低于对照组(P＜O.01，P＜0．05)；培养48小时CD^ 25细胞百分率显著低于对照组(P＜O．01)；培养48小时淋巴细胞凋亡率与CD^ 25细胞百分率呈负相关(P＜0．05)。认为HSP患儿外周血淋巴细胞凋亡过度，此与其T淋巴细胞免疫应答活性低下关系密切。     

Autolysosomes accumulate during in vitro CD8+ T-lymphocyte aging and may participate in induced death sensitization of senescent cells

As autophagic inclusions accumulate in senescent fibroblasts, we wondered whether an increase in cellular fragility during in vitro lymphocyte aging may be related to an autolysosome accumulation. We established that, during long-term cultures, repeatedly stimulated T-lymphocytes acquired characteristics of replicative senescence and became progressively intolerant to activation. Cell death following stimulations: (i) corresponded to apoptosis, associated with necrosis at the end of the culture; (ii) was not, for its main part, mediated through CD95/CD178 or TNFRII/TNF alpha interactions; and (iii) occurred in spite of bcl-2 increased expression. After 14 weeks of culture, the percentage of lymphocytes containing at least one autophagic inclusion (p<0.0001) and the lipofuscin autofluorescence in lymphocytes (p<0.0001) were significantly increased. The expression of several genes regulating autophagy did not significantly vary with the age of the culture. Forty-eight hours after each stimulation, the percentage of induced cell death rose while, in the remaining living cells, the percentage of lymphocytes with autophagic vacuoles (p<0.05), with beta-galactosidase activity and the lipofuscin autofluorescence (p<0.001) significantly decreased, suggesting the preferential death of cells with autophagy. Our data support the view that the accumulation of autolysosomes in senescent lymphocytes might aggravate cellular fragility, leading to apoptosis and necrosis mainly induced by lymphocyte activation.     

丹参对衰老鼠脑海马神经细胞凋亡作用的研究

目的：研究丹参对衰老鼠脑海马神经细胞凋亡的作用。方法：用TUNEL法及流式细胞仪观察衰老鼠的神经细胞凋亡,并用免疫组织化学法检测相关基因表达变化。以丹参注射液干预衰老的大鼠模型,观察了丹参对衰老鼠神经细胞凋亡的作用。结果：衰老鼠海马细胞有典型的凋亡特征,与丹参组比较海马细胞的凋亡率有明显差异,衰老鼠bcl-2表达下调,bax的表达量明显增加,基因表达变化与流式细胞仪测定的细胞凋亡率一致。结论：丹参对衰老鼠的脑神经细胞凋有明显的抑制作用。     

Relationship between oxidative stress and apoptotic markers in lymphocytes of diabetic patients with chronic non healing wound

Aims

Hyperglycemia causes generation of free radicals which leads to oxidative stress and apoptosis in various cells. The present study was undertaken to investigate the correlation between oxidative stress and apoptotic markers in lymphocytes of diabetic patients with chronic non healing wounds.

Methods

Thirty healthy, thirty uncontrolled type 2 diabetes mellitus (T2DM) and thirty uncontrolled T2DM with chronic, non healing, neuropathic diabetic foot patients were included in this study. Indices of oxidative stress inside the lymphocyte lysate were estimated by measuring content of superoxide dismutase (SOD), Catalase, Glutathione and malonaldialdehyde (MDA). Protein expression studies of pro and anti apoptotic markers were carried out to elucidate their possible involvement in diabetic context.

Results

SOD and MDA activity was significantly higher in the lymphocytes of diabetic patients having chronic, non healing diabetic wound as compared with healthy (p < 0.001); whereas catalase and GSH activity was significantly reduced (p < 0.001) in the same group. Expressions of pro apoptotic markers (Caspase-3, Fas and Bax) were significantly higher whereas reduced expression of anti-apoptotic marker (Bcl-2) were obtained in lymphocytes of diabetic and non diabetic individuals.

Conclusions

Hyperglycemia confers pro apoptotic manifestations which are mostly through altered indices of oxidative stress within lymphocytic milieu.     

Apoptosis and B-cell lymphoma-2 of peripheral blood T lymphocytes and soluble fas in patients with allergic asthma

STUDY OBJECTIVE:s: The dysregulation of apoptosis and the expression of apoptosis-related molecules of allergen-reactive T lymphocytes have been suggested to play a key role in the development and maintenance of the inflammatory reactions in allergic asthma. Glucocorticoids are effective drugs for treating allergic inflammation. In this study, we investigated the effect of dexamethasone (DEX) on the apoptosis and B-cell lymphoma (Bcl)-2 expression of peripheral blood T lymphocytes as well as the soluble form of Fas (sFas) in allergic asthmatic patients. METHODS: Peripheral blood lymphocytes from 41 allergic asthmatic patients and 30 age-matched and sex-matched control subjects were treated with 0.1 and 1 micro M DEX. The percentages of apoptosis and expression of the Bcl-2 molecule in T lymphocytes were assessed by flow cytometry. The plasma concentration of sFas was measured using the enzyme-linked immunosorbent assay. RESULTS: DEX (0.1 and 1 micro M) could induce the apoptosis of T lymphocytes from allergic asthmatic patients and control subjects in a dose-dependent manner in vitro. The apoptotic susceptibility of T lymphocytes to DEX and the plasma sFas concentration were significantly higher in allergic asthmatics. The ex vivo expression of Bcl-2 was significantly lower in the T lymphocytes of asthmatic patients than in those of the control subjects. However, DEX did not have any significant effect on the expression of Bcl-2 in vitro. CONCLUSIONS: The T lymphocytes of asthmatic patients have higher apoptotic susceptibility to DEX treatment in vitro and a lower expression of the Bcl-2 molecule.     

Age-related susceptibility of naive and memory CD4 T cells to apoptosis induced by IL−2 deprivation or PHA addition

The increased age-associated incidence of infectious and cancer diseases has been related to the alteration of immune functioning found in the elderly (immunosenescence). The reduction of naive T cells, which determine an impaired ability to mount immune responses to new antigens, represents a hallmark of the aging process. The aim of this study was to evaluate the susceptibility to apoptosis of purified naive and memory CD4⁺ T cells from peripheral blood of healthy people ranging in age from 20 to 98 years. Two mechanisms of T cell elimination by apoptosis have been evaluated: cytokine deprivation and activation-induced cell death. After Interleukin−2 deprivation, the percentage of naive and memory CD4⁺ apoptotic cells significantly increased with donor age concomitantly with a reduction of Bcl-2 expression and an increase of intracellular content of reactive oxygen species. After phytohemagglutinin addition, the percentage of apoptotic cells, the expression of CD95, and the intracellular reactive oxygen species, were not significantly correlated with age both in naive and memory CD4⁺ T cells. Our data demonstrate the existence of functional alterations of naive and memory T cell populations during ageing. These alterations are mainly related to the mechanism of the apoptotic event rather than to the type of cell population involved (naive or memory). The alterations of naive and memory T cells may have implications in the age-related susceptibility to diseases.