肾移植患者外周血中的CD4+ CD25+ CD127low/-调节性T细胞

背景：越来越多的实验在分析免疫耐受标志,以期能够更好地辅助患者进行移植后免疫抑制治疗。 目的：分析肾移植后患者外周血中CD4+ CD25+ CD127low/-调节性T细胞在肾移植免疫耐受中的作用。 方法：采集62例肾移植后患者(急性排斥反应组22例,移植稳定组40例)及20例健康对照者的外周抗凝血,经免疫染色,应用流式细胞仪分析CD4+ CD25+ CD127low/-调节性T细胞所占CD4+ T细胞百分含量,同时采用ELISA方法检测患者血清中白细胞介素2和白细胞介素10的质量浓度。 结果与结论：移植稳定组中CD4+ CD25+ CD127low/-调节性T细胞所占CD4+ T细胞百分含量显著高于健康对照组和急性反应排斥组(P < 0.01);CD4+ CD25+ CD127low/-调节性T细胞百分含量与白细胞介素2呈显著负相关(P < 0.05),与白细胞介素10呈显著正相关(P < 0.01)。提示CD4+ CD25+ CD127low/-调节性T细胞在肾移植后免疫耐受的机制中发挥了一定作用。     

糖皮质激素对多发性硬化患者外周血淋巴细胞CD80和CD4+CD25+T细胞表达的影响

目的探讨糖皮质激素(GC)对多发性硬化(MS)患者外周血淋巴细胞CD80和CD4+CD25+T细胞表达的影响。方法利用流式细胞仪检测21例MS急性期患者GC治疗前后外周血淋巴细胞CD80和CD4+CD25+T细胞阳性率,并与正常对照组比较;比较MS患者治疗前后扩展功能障碍状况量表(EDSS)评分的变化。结果MS患者急性期外周血淋巴细胞CD80的阳性率[(5.031±1.782)%]较正常对照组[(6.436±2.035)%]明显下降(P<0.05),经GC治疗后CD80的阳性率[(6.467±1.882)%]明显增高(P<0.01);CD4+CD25+T细胞阳性率治疗前后与正常对照组间差异均无统计学意义;治疗后EDSS评分[(3.64±1.79)分]较治疗前[(4.26±1.68)分]明显下降(P<0.01)。结论GC可上调MS患者淋巴细胞CD80的表达,抑制细胞免疫,促进MS病情缓解。     

首发精神分裂症和首发抑郁症患者血浆白细胞介素及其可溶性受体的对照研究

目的 在细胞因子水平探讨精神分裂症和抑郁症病理机制的异同.方法 首发精神分裂症和首发抑郁症患者各30例,分别单一接受利培酮(6 mg/d)、帕罗西汀(20 mg/d)治疗6周,治疗前后用阳性和阴性症状量表(PANSS)评估精神分裂症患者,并用汉密尔顿抑郁量表(HAMD)评估抑郁症患者.用酶联免疫吸附(ELISA)法测定治疗前后患者组和30名正常对照的血浆白细胞介素2(IL-2)、可溶性白细胞介素-2受体(slL-2R)、白细胞介素-6(IL-6)、可溶性白细胞介素-6受体(sIL-6R)的浓度.结果 ①治疗前,2个患者组的血浆IL-2、sIL-2R、IL-6、sIL-6R均高于正常对照组(P<0.05);精神分裂症组血浆sIL-2R高于抑郁症组(P<0.05),而IL-2、IL-6、sIL-6R低于抑郁症组(P<0.05).②治疗后,精神分裂症组血浆IL-2、sIL-6R较治疗前下降(P<0.05),抑郁症组血浆IL-2、sIL-2R、IL-6、sIL-6R均较治疗前下降(P<0.05);精神分裂症组血浆sIL-2R高于抑郁症组(P<0.05).而IL-2、sIL-6R低于抑郁症组(P均小于0.05).③精神分裂症组治疗前后血浆IL-2变化率与PANSS总分减分率正相关(r=0.64,P<0.001);抑郁症组治疗前后血浆IL-2和IL-6的变化率均与HAMD总分减分率正相关(r=0.42,P:0.02;r=0.54,P=0.002).结论 精神分裂症和抑郁症细胞因子均存在异常,提示二者可能存在共同的病理机制,但细胞因子表达的差异可能与二者存在不同的生物学基础有关.     

脑外伤SIRS患者外周血中IL-2、IL-6的临床观察

目的探讨颅脑损伤后全身炎症反应综合征(SIRS)患者外周血IL-2、IL-6表达的临床意义。方法56例符合SIRS诊断的颅脑损伤患者按GCS分为重型、中型和轻型3组,入院24h内进行SIRS评分,同时采取双抗体夹心ELISA法检测外周血IL-2、IL-6含量,并进行组间比较,同时与GCS评分、SIRS评分进行相关性分析。结果轻型、中型和重型组血中IL-2含量分别是(558.9±219.6)μ/ml、(614.2±209.6)μ/ml和(904.5±401.37)μ/ml,重型组明显高于中型和轻型组(P<0.05)。轻型组、中型组和重型组血中IL-5含量分别是(10.39±7.66)pg/ml、(26.75±14.68)pg/ml和(45.8±17.24)pg/ml,各组间有非常显著差异(P<0.01)。GCS评分及SIRS评分均与IL-2、IL-6呈显著负相关(P<0.01)。预后差的患者的IL-2、IL-6含量显著高于全组病人的水平(P<0.01)。结论IL-2、IL-6在颅脑损伤后SIRS患者外周血中有较高的表达,可能是引起SIRS的因素之一。     

重症肌无力患者外周血CD4+T细胞OX40的表达及作用机制研究

目的 分析重症肌无力(MG)患者外周血CD4+T细胞协同刺激分子OX40表达及其对FoxP3+CD4+CD25+调节性T细胞(Treg)的调控作用,初步探讨OX40在MG免疫学发病中的作用机制.方法 以流式细胞技术检测42例MG患者及38名健康对照的外周血OX40+CD4+T细胞、FoxP3+CD4+CD25+Treg表达水平,比较OX40表达在MG患者不同临床疾病状态、Osserman分型、临床绝对评分、胸腺病理类型等情况下的差异,并分析OX40对FoxP3+CD4+CD25+Treg细胞的影响.结果 (1) MG患者外周血OX40+CD4+T细胞占淋巴细胞百分比高于健康对照组(P<0.01).(2)MG患者OX40+CD4+T细胞百分比在发作或加重期高于缓解期(P＜0.05);在临床绝对评分呈中、重度患者OX40+CD4+T细胞百分比高于轻度患者(均P＜0.05);Osserman Ⅱ、Ⅳ型患者OX40+CD4+T细胞百分比高于Ⅰ型患者(均P＜0.05);胸腺增生及胸腺瘤患者OX40+CD4+T细胞百分比高于胸腺正常患者(P＜0.05,P＜0.01).(3)MG患者外周血OX40+CD4+T细胞百分比与FoxP3+CD4+CD25+Treg细胞百分比呈负相关(r=-0.843,P=0.01).结论 协同刺激分子OX40参与MG发病,可能通过抑制FoxP3+CD4+CD25+Treg细胞生成发挥作用.     

重症肌无力患者外周血调节性T细胞及B细胞激活因子受体的分析

目的 研究重症肌无力(MG)患者外周血多群调节性T细胞的水平及其B细胞表达B细胞激活因子受体(B cell-activating factor receptor,BAFF-R)的情况.方法 应用四色流式细胞仪检测61例MG患者与23名健康对照外周血调节性T细胞(CD4+ CD25 high Foxp3+、CD8+ CD28-、CD8+ CD122+)以及CD19+ BAFF-R+细胞的百分率.结果 MG组与健康对照组外周血CD4+ CD25 high Foxp3+ T细胞的百分率分别为32.12%±16.12%与65.15%±14.72%,MG组该群调节性T细胞的水平明显低于健康对照组(P＜0.01);两组CD8+ CD28-及CD8+ CD122+ T细胞的水平差异无统计学意义.此外,MG组外周血CD19+ BAFF-R+细胞的水平(10.57%±5.59%)显著高于健康对照组(5.38%±3.87%,P＜0.01).大剂量激素或大剂量激素加丙种球蛋白治疗后短期内可使MG组外周血CD4+ CD25 high Foxp3+调节性T细胞的百分率增加(P＜0.05).结论 MG患者Foxp3+的CD4+ CD25 high调节性T细胞的减少提示MG患者存在免疫和耐受的失衡,显示了T细胞的自身免疫性.在B细胞方面,MG患者外周血CD19+ B细胞上BAFF-R表达增高,提示其体内B细胞已处于易激活状态.     

CD4~+、CD25~+、CD127 low调节T细胞及CD16~+、CD56NK细胞在脑梗死急性期患者外周血中的表达及其关系

目的探讨脑梗死(CI)患者外周血中CD4+、CD25+、CD127 low调节T细胞及CD16+、CD56NK细胞的百分比变化及两者在CI患者免疫反应中的相互作用机制。方法采用流式细胞术检测50例急性CI患者(发病2d)外周血中CD4+、CD25+、CD127 low调节T细胞及CD16+、CD56NK细胞的表达水平,并与健康对照组进行比较。结果急性CI患者(发病2d)外周血中的CD4+、CD25+、CD127 low调节T细胞的表达水平低于健康对照组,而CD16+、CD56NK细胞的数量则明显高于健康对照组(p<0.05)。结论急性CI患者发病2d,CD16+、CD56NK细胞表达水平上升,而CD4+、CD25+、CD127 low调节性T细胞表达明显低于健康对照组,说明CD4+、CD25+、CD127 low调节性T细胞和CD16+、CD56NK细胞是促进CI发生的原因之一。     

老年与中青年脑梗死患者淋巴细胞亚群的对比研究

目的探讨不同年龄阶段脑梗死患者与淋巴细胞亚群的关系。方法选择101例临床确诊的急性脑梗死(ACI)患者,分成老年ACI组(66例)和中青年ACI组(35例)。选择对照组50例,应用流式细胞分析仪检测ACI患者和对照组外周血中淋巴细胞亚群相对计数。结果①老年脑梗死患者与正常对照组比较:CD8+T和CD19+B细胞百分率升高差异有统计学意义(P<0.05);CD4/CD8和CD4+T细胞百分率降低差异有统计学意义(P<0.05);CD3+T细胞百分率变化不明显(P>0.05)。②中青年脑梗死患者与正常对照组相比较:CD4+T细胞百分率和CD4/CD8降低差异有统计学意义(P<0.05);而CD3+T、CD8+T和CD19+B细胞百分率变化不明显(P>0.05)。③老年ACI组患者与中青年ACI组患者比较:CD8+T和CD19+B细胞百分率升高差异有统计学意义(P<0.05);CD3+T、CD4+T细胞百分率和CD4/CD8比较变化不明显(P>0.05)。结论 ACI患者体内淋巴细胞亚群发生重新分布,尤其老年ACI淋巴细胞亚群变化显著,这为我们在临床治疗中提供了新的思路。     

帕金森病大鼠CD4+CD25highFoxP3+调节性T细胞的变化

目的 研究帕金森病(Parkinson's disease,PD)大鼠外周血中调节性T细胞(regulatory T cells,Treg)的改变,并探讨其与脑内免疫炎症反应的相关性.方法 SD大鼠随机分为对照组、假手术组、PD 4周组、PD 2周组.PD 4周组和2周组定向注射6-羟多巴建立PD大鼠模型,假手术组注射PBS缓冲液,PD 2周组于术后第2 周,其他组于术后第4 周时,应用免疫荧光染色法观察各组大鼠黑质处酪氨酸羟化酶(Tyrosine hydroxylase,TH)阳性神经元、离子钙接头蛋白分子-1(Ionized calcium bindingadaptor molecule-1,iba-1)和胶原纤维酸性蛋白(Glial fibrillary acid protein,GFAP)阳性细胞数量及形态的改变,并通过流式细胞术(Flow cytometry,FCM)检测其外周血中CD4+CD25highFoxP3+ Treg 占T 淋巴细胞比例的变化.结果 PD4 周组TH 阳性神经元偏侧毁损率(91.33%±8.53%)较对照组和假手术组增加(P<0.01),且较PD2周组(64.56%±17.94%)毁损更为严重(P<0.05).PD4周组iba-1阳性细胞增加率(82.60%±11.52%)和GFAP阳性细胞增加率(86.62%±6.80%)较对照组及假手术组均增加(P<0.01),但PD 4 周组较2 周组iba-1 阳性细胞增加率(104.89%±13.39%)和GFAP 阳性细胞增加率(117.92%±15.34%)均减少(P<0.05).FCM示PD4周组大鼠外周血中CD4+CD25highFoxP3+ Treg占T淋巴细胞的比例(0.64%±0.08%)较对照组、假手术组及PD2周组均降低(P<0.01).另外,外周血T淋巴细胞中Treg比例变化与TH 阳性神经元毁损率(r=-0.59,P<0.01)、iba-1 阳性细胞增加率(r=-0.87,P<0.01)和GFAP 阳性细胞增加率(r=-0.89,P<0.01)均呈负相关.结论 PD大鼠外周血中Treg比例减少且可能与脑内免疫炎症反应相关.     

抑郁症中糖皮质激素受体与CD4+CD25+调节性T细胞的关系及其所致免疫失衡机制的初步探讨

目的 研究抑郁症患者外周血细胞因子白介素-10(IL-10)、转化生长因子β(TG-β)的变化、CD4+CD25+调节性T细胞(Treg)的数量及其特征性标志叉头样转录因子P3(Foxp3)的表达与糖皮质激素受体(GR)的表达之间的关系,探讨抑郁症患者免疫失衡的可能机制.方法 纳入36例抑郁症患者和36名正常对照,根据Hamilton抑郁量表总分将患者划分为轻、中和重不同抑郁程度组;利用ELISA方法测定受试者外周血血清细胞因子IL-10、TGF-β浓度;逆转录-聚合酶链反应(RT-PCR)检测GR的α及β两种亚型(GRα、GRβ)、Foxp3 mRNA表达水平;免疫磁珠分离CD4+ CD25+ Treg,共聚焦显微镜观察Foxp3与GR在CD4+CD 25+ Treg上的共表达.结果 与正常对照组比较,患者组血清IL-10、TGF-β的水平降低(P＜0.05),外周血CD4+ CD25+ Treg数量及在CD4+T细胞中的比例明显少于对照组(P＜0.01),且重度抑郁组上述指标明显低于中度和轻度抑郁组(P＜0.01).抑郁各组单个核细胞GRamRNA和FoxP3 mRNA表达水平随抑郁程度而降低(P＜0.01),GRβmRNA却在重度抑郁组表达增加.共聚焦显微镜下可观察到重度抑郁患者CD4+CD25+Treg上GR与Foxp3表达显著减少.结论 糖皮质激素受体可能通过影响调节性T细胞的功能和数量在抑郁症患者免疫失衡的病理生理机制中发挥着重要的作用.     

Functional assay for human CD4+CD25+ Treg cells reveals an age-dependent loss of suppressive activity

CD4+CD25+ regulatory T cells (Treg cells) prevent T cell-mediated autoimmune diseases in rodents. To develop a functional Treg assay for human blood cells, we used FACS- or bead-sorted CD4+CD25+ T cells from healthy donors to inhibit anti-CD3/CD28 activation of CD4+CD25- indicator T cells. The data clearly demonstrated classical Treg suppression of CD4+CD25- indicator cells by both CD4+CD25(+high) and CD4+CD25(+low) T cells obtained by FACS or magnetic bead sorting. Suppressive activity was found in either CD45RO- (naive) or CD45RO+ (memory) subpopulations, was independent of the TCR signal strength, required cell-cell contact, and was reversible by interleukin-2 (IL-2). Of general interest is that a wider sampling of 27 healthy donors revealed an age- but not gender-dependent loss of suppressive activity in the CD4+CD25+ population. The presence or absence of suppressive activity in CD4+CD25+ T cells from a given donor could be demonstrated consistently over time, and lack of suppression was not due to method of sorting, strength of signal, or sensitivity of indicator cells. Phenotypic markers did not differ on CD4+CD25+ T cells tested ex vivo from suppressive vs. nonsuppressive donors, although, upon activation in vitro, suppressive CD4+CD25+ T cells had significantly higher expression of both CTLA-4 and GITR than CD4+CD25- T cells from the same donors. Moreover, antibody neutralization of CTLA-4, GITR, IL-10, or IL-17 completely reversed Treg-induced suppression. Our results are highly consistent with those reported for murine Treg cells and are the first to demonstrate that suppressive activity of human CD4+CD25+ T cells declines with age.     

应用供体抗原特异性CD4+CD25+ Treg细胞延长大鼠移植肾的存活

背景：随着磁分选技术的完善,体外分选、扩增足量的对移植抗原具有特异性的细胞已成为可能,但就其在体内应用剂量及免疫耐受的效能问题目前鲜有报道。 目的：探索供体抗原特异性CD4+CD25+Treg细胞在体内应用诱导移植免疫耐受的量效关系。 方法：以SD大鼠为供体、Wistar大鼠为受体,建立同种异体肾移植动物模型;体外分选、富集Wistar大鼠脾脏CD4+CD25+Treg细胞,并诱导其对SD大鼠供体抗原的特异性表型;根据不同数量(2×105、5×105、1×106、2×106)供体抗原特异性CD4+CD25+Treg细胞在肾移植中单剂量尾静脉注射,并以未注射组为对照。术后15 d分析移植肾脏存活状况。术后4,9,15 d采血检测各组肌酐水平,同时进行移植肾脏病理检查,按照Banff Schema标准进行诊断,并根据Watanabe的方法进行半定量评分。 结果与结论：术后15 d内对照组死亡率最高83.3%,2×105组次之66.7%,2×106组为58.3%,5×105组为33.3%,1×106组则全部存活;各实验组术后4,9,15 d血肌酐水平均明显低于对照组(P < 0.05,P < 0.01);术后第9,15天,2×105组、5×105组血肌酐水平均明显高于1×106组、2×106组(P < 0.05);术后第4,9,15天移植肾脏病理检查的半定量评分结果显示,各时间段5×105组、2×105组与对照组间差异无显著性意义,各时间段1×106组与2×106组优于对照组 (P < 0.05)。结果初步证实供体抗原特异性CD4+CD25+Treg细胞受体内应用能够改善大鼠移植肾功能,延长移植肾存活时间,1×106为相对理想的单次应用剂量。     

外周血CD4+CD25highTreg细胞的比例变化在肾移植受者术后免疫监测中的临床应用研究

目的 研究外周血CD4+CD25highTreg细胞(regulatory T cell,Treg)比例对肾移植受者免疫力的影响,为CD4+CD25highTreg细胞的比例变化作为评估移植受者免疫状态及作为预测排斥反应和感染的特异性指标提供实验依据。方法 肾移植受者52例按肾移植术后恢复情况分为免疫力正常组26例,发生排斥反应组17例,发生感染组9例,用流式细胞仪检测外周血CD4+CD25highTreg细胞的比例,所得结果进行相关分析。结果 发生急性排斥反应组CD4+CD25highTreg细胞比例较免疫力正常组显著降低（p〈0.05）,发生感染组外周血CD4+CD25highTreg细胞的比例较正常组显著升高（p〈0.01）,均有统计学意义。FK-506和CsA分别对CD4+CD25highTreg细胞比例的影响没有显著性差异。结论 肾移植术后受者外周血CD4+CD25highTreg细胞比例与受者免疫状态密切相关。CD4+CD25highTreg细胞比例的变化可以反应机体的免疫状态的变化,其升高或降低可以作为预测肾移植受者术后发生感染或排斥反应的指标之一。     

Multiple sclerosis: a study of chemokine receptors and regulatory T cells in relation to MRI variables

Magnetic resonance imaging (MRI) remains the most valuable tool for monitoring disease activity and progression in patients with multiple sclerosis (MS), a chronic demyelinating disease of the central nervous system (CNS) with presumably autoimmune etiology. Chemokine receptors have been implicated in MS as key molecules directing inflammatory cells into the CNS. Regulatory (CD4+CD25+) T cells (Tr cells) are important in suppressing autoimmunity, and their absolute or functional deficit could be expected in MS. In the present study, venous blood was obtained from MS patients concurrent with MRI examination of the brain, and expression of chemokine receptors CCR1, CCR2, CCR5, CXCR3 and CXCR4 by CD4 T cells and monocytes, proportions of Tr cells, as well as expression of CD45RO, CD95, CTLA-4, HLA-DR and interleukin (IL)-10 by Tr cells and non-Tr (CD25-) CD4 T cells was analyzed by flow cytometry. Surface expression of CXCR3 by CD4 T cells was downregulated in the group of patients with high lesion load (LL) on T2-weighted images and gadolinium (Gd)-enhancing lesions on T1-weighted images, compared to the group with high LL and no Gd-enhancing lesions, and to the group with low LL, suggesting internalization of CXCR3 due to the release of its chemokine ligand (IP-10/CXCL10) from active MS lesions. Proportions of Tr cells amongst all CD4 T cells, and expression of IL-10 by Tr cells were increased in the patients with high LL and Gd-enhancing lesions. These results suggest that there is correlation between MRI parameters, chemokine receptor expression and the status of circulating Tr cells in MS, but further studies need to discriminate between pathogenetically relevant and bystander phenomena.     

Decreased production of interleukin-2 (IL-2), IL-2 secreting cells and CD4+ cells in medication-free patients with schizophrenia

There are a number of indications that schizophrenia is associated with changes in the immune system. Although functional studies have mostly demonstrated decreased in vitro production of IL-2 by peripheral blood mononuclear cells (PBMCs) stimulated with mitogen, the reason is unclear. The aim of the study was to explore the relationship between IL-2 production and CD4+ cells which mainly secret IL-2 in non-Caucasian patients with schizophrenia. Blood CD4+ cells and mitogen-stimulated IL-2 secreting cells identified by an immunohistochemical study with the alkaline phosphatase/anti-alkaline phosphatase (APAAP) technique, and in vitro IL-2 production with radioimmunometric assay (RIA) were measured in 30 schizophrenic patients and 30 normal control subjects matched for sex, age and race. The results showed that blood CD4+ cells and mitogen-induced IL-2 secreting cells and IL-2 production were significantly lower in schizophrenic subjects than in the normal controls. There was significantly positive correlation between CD4+ cells and IL-2 production in normal controls but not in patients. These findings suggest that immune disturbance may be present in schizophrenic patients. The lower in vitro IL-2 production is probably related to the decreased number of T-cells that secret IL-2, as well as to the intrinsic disorder of the patients' T cells.     

Immunotherapy of rat glioma without accumulation of CD4~+CD25~+FOXP3~+ regulatory T cells

Immunotherapy may be used for the treatment of glioblastoma multiforme;however,the induced immune response is inadequate when either T cells or dendritic cells are used alone.In this study,we established a novel vaccine procedure in rats,using dendritic cells pulsed with C6 tumor cell lysates in combination with adoptive transfer of T lymphocytes from syngenic donors.On day 21 after tumor inoculation,all the rats were sacrificed,the brains were harvested for calculation of glioma volume,cytolytic T lymphocyte responses were measured by cytotoxic assay,and the frequency of regulatory T lymphocytes(CD4+CD25+FOXP3+) in the peripheral blood was investigated by flow cytometric analysis.The survival rate of rats bearing C6 glioma was observed.Results showed that the co-immunization strategy had significant anti-tumor potential against the pre-established C6 glioma,and induced a strong cytolytic T lymphocyte response in rats.The frequency of peripheral blood CD4+CD25+FOXP3+ regulatory T lymphocytes was significantly decreased following the combination therapy,and the rats survived for a longer period.Experimental findings indicate that the combined immunotherapy of glioma cell lysate-pulsed dendritic cell vaccination following adoptive transfer of T cells can effectively inhibit the growth of gliomas in rats,boost anti-tumor immunity and produce a sustained immune response while avoiding the accumulation of CD4+CD25+FOXP3+ regulatory T lymphocytes.     

大鼠脑局灶缺血／再灌注对外周血单个核CD34^＋细胞的影响

目的本研究探讨大鼠脑局灶缺血/再灌注是否影响外周血单个核CD34+细胞的数量.方法采用大鼠大脑中动脉(MCA)缺血/再灌注线栓法模型,将大鼠随机分为3组对照组,假手术组,动物模型组.取再灌注后1、3、6、12 h和1、2、3、4、7、14 d,10个观察点,测外周血单个核CD34+表达情况.结果大鼠脑缺血/再灌注模型中外周血单个核CD34+细胞在再灌注后1 h～2 d无明显变化,在脑缺血/再灌注后3～7 d明显减少,14 d后恢复.结论大鼠脑缺血/再灌注模型再灌注后1 h～2 d再灌注后外周血单个核CD34+细胞没有变化,在脑缺血/再灌注后3～7 d明显减少.     

Immune disturbances during major depression: upregulated expression of interleukin-2 receptors

We determined the following immune parameters in drug-free, major depressed patients and in age- and sex-matched healthy controls: the number and percentage of interleukin-2 receptor (IL-2R) bearing cells (CD25+, anti-TAC), serum circulating levels of soluble (s)IL-2Rs, the pre- and postdexamethasone phytohemagglutinin (PHA)-induced accumulation of sIL-2Rs in culture supernatant, and the number of T helper (CD4+) and T suppressor (CD8+) cells. In comparison with normal volunteers, patients with major depression had a higher number and percentage of CD25+ cells, higher concentrations of serum circulating sIL-2Rs, higher supernatant sIL-2Rs after stimulation with PHA, and a higher number of CD4+ cells. The CD4+/CD8+ ratio and the number of CD4+ cells were significantly and positively related to the number of cells expressing the CD25+ antigen. These results may indicate that depressed patients display an increased number of T cells in an early phase of activation.     

Preferential increase of IL-2R+ CD4+ T cells and CD45RB- CD4+ T cells in the central nervous system in experimental allergic encephalomyelitis.

We examined lymphocytes isolated from the spinal cord (SC), peripheral blood (PB) and lymph nodes (LN) draining the immunization site of Lewis rats with acute experimental allergic encephalomyelitis (EAE). Cells were analysed for T cell subset markers CD4 (mAb W3/25) and CD8 (mAb OX8), for IL-2R (mAb OX39), and for high molecular mass leukocyte common antigen (LCA, CD45RB) expression (mAb OX22). T cells expressing high (CD45RB+) or low (CD45RB-) molecular mass LCA are of different maturational stages and/or separate lineages. CD4+ T cells were more predominant in SC than in PB and LN; CD8+ T cells were scarce in SC but common in PB and LN. Activated CD4+ T cells (IL-2R+) were common in the SC and LN but infrequent in blood. CD4+ T cells that were CD45RB+ were scarce in the SC. In contrast, the majority of CD4+ T cells in the PB and LN were CD45RB+. The preferential accumulation of IL-2R+ CD4+ T cells and of CD45RB- CD4+ T cells in the central nervous system (CNS) indicates that a selective mechanism directs cell egress into CNS lesions in EAE.