寻常型银屑病患者外周血CD4~+CD25~+及CD8~+CD25~+细胞的检测

目的研究进展期寻常型银屑病患者外周血CD4+CD25+和CD8+CD25+调节性T细胞的数量变化及其在银屑病免疫病理学发病机制中的作用。方法应用流式细胞术对进展期寻常型银屑病患者外周血CD4+CD25+和CD8+CD25+调节性T细胞进行检测。结果进展期寻常型银屑病外周血CD4+CD25+细胞及CD8+CD25+调节性T细胞数量与正常对照组相比,均显著降低(P<0.05,P<0.005),而CD4+CD25+/CD8+CD25+比值无显著性差异(P>0.05)。结论寻常型银屑病的发病与CD4+CD25+和CD8+CD25+调节性T细胞的同步降低有关,与二者的比值无关。     

Imbalance of CD4+CD29+ and CD4+CD45RA+ T-helper cell subsets in peripheral blood of patients with severe atopic dermatitis

To determine the proportion of T-helper cell subsets in the peripheral blood we studied 16 patients with mild, moderate and severe atopic dermatitis. Lymphocytes were isolated from heparinized peripheral blood and analysed by two-colour flow cytometry. Patients with severe atopic dermatitis had a decreased CD4+CD29+CD4+CD45RA+ ratio (p<0.01). We found a decreased absolute number of CD4+CD29+ cells (p<0.05) and an increased absolute number of CD4+CD45RA+ cells (p<0.05) in the peripheral blood. No significant changes in the CD4+CD29+CD4+CD45RA+ ratio were found in the peripheral blood of patients with clinically mild or moderate atopic dermatitis.     

226例HIV-1抗体阳性者WB带型及首次CD4+T淋巴细胞检测结果分析

目的:通过分析HIV-1抗体阳性者WB带型及首次CD4+T淋巴细胞检测结果,总结条带出现规律,探索疾病进展与免疫状况,为疾病分期提供依据.方法:运用WB试验确证226例HIV-1阳性者,流式细胞仪检测CD4+T淋巴细胞,统计WB带型及不同疾病分期CD4+T淋巴细胞计数.结果:226例HIV-1抗体阳性者中男性占79.6...     

梅毒患者外周血CD4~+、CD8~+调节性T细胞表达的临床意义

目的:监测梅毒患者外周血CD4~+、CD8~+调节性T细胞的表达水平,考察其在临床的参考价值。方法:将2014年12月至2015年9月,我院收治并确诊的32例梅毒患者作为研究对象。其中,Ⅰ期、Ⅱ期、潜伏期梅毒患者分别有11例、15例和6例。采用细胞免疫芯片检测(淋巴细胞CD4~+、CD8~+绝对数检测)技术检测并计算患者外周血中的调节性T细胞CD4~+、CD8~+表达水平及CD4~+、CD8~+的比值。并与同期就诊我科的30例非梅毒患者的相应指标数据进行比较。结果:与非梅毒患者比较,梅毒患者外周血中CD4~+、CD8~+细胞绝对值计数均显著下降(P0.05);CD4~+、CD8~+比值显著低于非梅毒患者组(P0.05)。在Ⅰ期、Ⅱ期、潜伏期梅毒患者间CD4~+、CD8~+绝对值计数均值水平的差异有统计学意义(P0.05)。结论:在梅毒患者外周血中CD4~+、CD8~+表达水平及CD4~+、CD8~+比值均显著降低,而在梅毒感染的不同疾病发展时期CD4~+、CD8~+表达水平也有着显著的差异。     

SLE患者外周血单一核细胞淋巴细胞功能相关抗原1表达的检测

目的 研究SLE患者外周血单一核细胞（PBMC）淋巴细胞功能相关抗原1（LFA-1）的表达,探讨LFA-1与SLE的发病及病情变化的关系及其临床意义。方法 提取30例SLE患者（SLE组）和24例正常人（对照组）的PBMC,用抗人CD3-FITC和抗人CD11a-PE对其进行标记后,采用流式细胞术检测其CD11a的表达率。结果 PBMC CD11a的表达率对照组为68.21% ± 4.58%,SLE组为73.74% ± 7.89%,活动期组为77.11% ± 7.46%,稳定期组为69.33% ± 6.27%,SLE组PBMC CD11a的表达率显著高于对照组（P ＜ 0.05）,且活动期组亦显著高于对照组（P ＜ 0.05）,而稳定期组与对照组比较,差异无统计学意义（P > 0.05）。活动期组与稳定期组比较,差异有统计学意义（P ＜ 0.05）。相关性分析显示,SLE患者CD11a的表达率与其采血时的SLEDAI呈正相关（r = 0.64,P ＜ 0.01）。结论 LFA-1的过表达参与SLE的发病,并与疾病活动相关。     

卵巢癌患者腹水及外周血CD4~+CD25~+调节性T细胞含量及抑制功能的研究

目的:分析并探讨卵巢癌患者腹水及外周血CD4~+CD25~+调节性T细胞含量及抑制功能。方法:选取2012年2月至2015年2月期间在我院和宁波市鄞州第二医院接受治疗的卵巢癌患者56例,采集腹水标本56例,外周血标本56例。使用流式细胞术检测CD4~+CD25~+调节性T细胞(Treg)的表达。采用1.5μmol/L的羧基荧光素二醋酸盐琥珀酰亚胺脂(CFSE)标记CD4~+CD25-T细胞,观察CFSE标记效果,计算抑制率。结果:研究结果显示,56例腹水患者CD4~+CD25~+T cells/CD4~+T cell为(28.34±13.27)%,56例外周血标本CD4~+CD25~+T cells/CD4~+T cell为(14.56±4.36)%。腹水和外周血标本CD4~+CD25~+T cells/CD4~+T cell含量有显著差异(P0.05)。腹水Treg抑制功能比外周血Treg强,经统计学检验,差异具有统计学意义(P0.05)。结论:腹水Treg含量及抑制功能比外周血Treg强,提示卵巢癌腹腔内相对容易发生免疫逃逸,而Treg升高可能参与促进肿瘤复发。     

艾滋病合并肺结核患者CD4+T淋巴细胞与肺结核类型的关系

目的探讨艾滋病合并肺结核患者CD4⁺T淋巴细胞的变化及意义。方法选取2014年6月至2019年6月在徐州医科大学附属沭阳医院治疗的93例艾滋病合并肺结核患者(艾滋病合并肺结核组),选取同期在徐州医科大学附属沭阳医院治疗的90例单纯肺结核患者(肺结核组)以及90例艾滋病未合并肺结核患者(艾滋病组)作为研究对象。检测三组的血清CD4+T淋巴细胞水平。结果艾滋病合并肺结核组、肺结核组和艾滋病组的CD4+T淋巴细胞水平分别为(92.21±16.68)个/mm³、(351.22±63.33)个/mm³和(240.41±30.21)个/mm³,艾滋病合并肺结核组明显低于肺结核组和艾滋病组(P<0.05),艾滋病组明显低于肺结核组(P<0.05);艾滋病合并肺结核组病变分类Ⅲ型患者CD4+T淋巴细胞水平为(85.66±17.03)个/mm³,明显低于Ⅰ型、Ⅱ型和Ⅳ型患者(P<0.05);Ⅱ型患者CD4+T淋巴细胞水平为(95.51±13.38)个mm³,明显低于Ⅰ型和Ⅳ型患者(P<0.05)。结论在艾滋病合并肺结核患者中,CD4⁺T淋巴细胞明显减少,与肺结核病变类型有一定关系。     

Functional characterization of CD4+CD25+ regulatory T cells differentiated in vitro from bone marrow-derived haematopoietic cells of psoriasis patients with a family history of the disorder

BACKGROUND: In psoriasis CD4+CD25+ regulatory T cells are functionally deficient. The imbalance between regulatory and effector T-cell functions is important for inducing psoriasis. It is reasonable to speculate that the dysfunctional activity of CD4+CD25+ regulatory cells may originate partly from the abnormal haematopoietic cells determined mainly by genetic background. OBJECTIVES: To test the hypothesis that haematopoietic stem cells are responsible for dysfunctional CD4+CD25+ regulatory cells in psoriasis. METHODS: Bone marrow-derived CD34+ haematopoietic cells from patients with psoriasis (with a family history of psoriasis) and from normal controls were differentiated into T cells in vitro. CD4+CD25+ T cells were isolated by an immunomagnetic bead method, and proliferation activity and capacity for cytokine secretion were determined. Furthermore, the ability of CD4+CD25+ T cells to suppress the proliferative responses of allogeneous peripheral blood CD4+CD25- effector T cells was assessed in vitro. RESULTS: The differentiated CD4+CD25+ T cells of psoriatic origin showed similar characteristics to those of normal volunteers, including proliferation activity and secretion profile of the cytokines interleukin (IL)-2, IL-4, IL-8, IL-10 and interferon (IFN)-gamma. However, proliferation and secretion levels of the cytokines IL-2 and IL-10 for CD4+CD25+ cells of psoriatic CD34+ cell origin were significantly lower than those of normal controls in response to streptococcal superantigen (Strep-A). In particular, CD4+CD25+ T cells differentiated from psoriatic CD34+ cells were functionally insufficient to restrain effector T-cell proliferation. CONCLUSIONS: CD4+CD25+ T cells differentiated in vitro from haematopoietic cells of patients with psoriasis are impaired in regulatory function. The dysfunction of psoriatic CD4+CD25+ T cells may be due to inherent genetic programming passed down from bone marrow-derived haematopoietic cells.     

外周血及蜕膜组织中CD4~+ CD25~+调节性T细胞比例和炎症因子原因不明复发性流产的关系研究

目的:探究外周血及蜕膜组织中CD4~+CD25~+调节性T细胞比例以及相关炎症因子对原因不明复发性流产的影响。方法:选取2014年5月至2015年5月就诊于我院门诊的原因不明复发性流产(URSA)患者90例为观察组,并选取同期在妇产科门诊手术室的行人工流产手术的正常患者90例为对照组;分析两组患者的一般资料、外周血及蜕膜组织中CD4~+CD25~+调节性T细胞比例、调节性T细胞特异调节因子Foxp3和EBi3的表达以及血清炎症因子(包括TNF-α、IL-2、IL-6、IL-10)水平,研究其相关性。结果:与正常妊娠组相比,反复流产组外周血及蜕膜组织中Treg细胞比例明显降低,Foxp3和EBi3因子mRNA的表达水平明显降低,且无论URSA患者或者是正常对照组,蜕膜中各因子的表达均高于外周血中的表达,外周血TNF-α、IL-2水平明显升高,而IL-6和IL-10水平要明显降低,差异有统计学意义(P0.05)。结论:蜕膜中各因子的表达均高于外周血中的表达提示妊娠过程的主要免疫反应部位是"母-胎界面",Treg细胞比例、Treg细胞因子和Th2型因子IL-6、IL-10水平可能参与妊娠的维持,调控"母-胎界面"局部免疫耐受。对于复发性流产的发病过程具有一定的影响作用。     

Epidermal CD8+ T cells in chronic plaque psoriasis are Tc1 cells producing heterogeneous levels of interferon-gamma

The majority of epidermal CD8+ T cells in chronic plaque psoriasis are activated Tc1 cells producing interferon-gamma and no interleukin-4, a small proportion of which express NK-T receptors. To quantitate their level of cytokine production and characterize them further, CD8+ T cells were isolated from epidermal cell suspensions of lesional biopsies from 24 patients with chronic plaque psoriasis. T-cell lines (TCL) were established by culture of CD8+ T cells with feeders and IL-2 for 11 days and expansion with PHA. Ten TCL were stained for surface markers; 6 were cloned with PHA by limiting dilution. Interferon-gamma, interleukin-4 and interleukin-10 production was measured by ELISA after PMA/anti-CD3 activation of 15 TCL and 39 CD8+ T-cell clones. The 10 TCL stained were CD8alphabeta+ (93.3%), T-cell receptor-alphabeta+ (99.5%), costimulatory molecule CD28+ (90.1%), with a small CD8alphaalpha+ population (2.3%). No NK-T-cell receptor CD158a or CD158b expression was detected, whilst CD94 was expressed on 6.2% of cells in 6/9 TCL. All the TCL and 37/39 CD8+ T-cell clones produced interferon-gamma but no or minimal interleukin-4 or interleukin-10. The TCL produced a wide range of interferon-gamma levels (138 to 15,020 pg/ml). Clones from 3 patients showed low levels (60 to 1,410 pg/ml), from 2 patients high levels (6,105 to 43,040 pg/ml) and from 1 patient a wide range (405 to 36,010 pg/ml) of interferon-gamma production. Thus epidermal CD8+ Tc1 cells in chronic plaque psoriasis produce highly heterogeneous levels of interferon-gamma, which may reflect clinical diversity.     

Persistent CMV infection correlates with disease activity and dominates the phenotype of peripheral CD8+ T cells in psoriasis

Background: Previously, we have reported a frequent association of active plaque psoriasis with inflammation‐mediated cytomegalovirus (CMV) reactivation. Objectives: This study aimed at characterizing the impact of CMV infection on psoriasis disease activity and peripheral cellular adaptive immune response. Patients/Methods: Twenty nine patients with active plaque psoriasis and 29 healthy controls were analysed for CMV‐serostatus, CMV‐antigenaemia, frequencies of peripheral CMV‐specific T cells and the immunophenotype of peripheral CD8+ T cells. Results: (i) Psoriasis severity was higher in CMV‐seropositive patients and positively correlated to the severity of CMV‐antigenaemia. (ii) In comparison to CMV‐seropositive healthy controls, CMV‐seropositive psoriasis patients showed a reduced frequency of circulating CMV‐specific T cells that increased under effective antipsoriatic therapy. (iii) The immunophenotype of peripheral CD8+ T cells was dominated by CMV‐seroprevalence. (iv) Selective analysis of CMV‐seronegative psoriasis patients revealed a strong expansion of a – probably early activated – CD8+ T‐cell population with the yet undescribed differentiation phenotype ‘CD45RA‐dim/CD11a‐dim’. Under effective antipsoriatic therapy this population decreased in parallel to an increase of effector differentiated CD8+ T cells. Conclusions: Taken together with our previous results of inflammation‐mediated CMV reactivation in psoriasis, our data support the concept of an interactive relationship between psoriasis and CMV infection which may be mediated by peripheral CD8+ T cells.     

Decreased suppression of CD8+ and CD4+ T cells by peripheral regulatory T cells in generalized vitiligo due to reduced NFATC1 and FOXP3 proteins

Regulatory T cells (Tregs) are involved in the suppression of activated T cells in generalized vitiligo (GV). The study was aimed to investigate Tregs functional defects in Treg:CD8⁺ and Treg:CD4⁺ T cells' co-culture systems of 55 GV patients and 45 controls. CD8⁺ and CD4⁺ T-cell proliferation was assessed by BrdU assay; production of IL-10, TGF-β and IFN-γ cytokines was assessed by ELISA; and FOXP3, CD25, NFATC1 and CD44 proteins were measured by flow cytometry. Generalized vitiligo patients showed reduced suppression of CD8⁺ and CD4⁺ T cells (P = .0384, P = .0084), increased IFN-γ (P < .0001, P = .0019), decreased IL-10 and TGF-β (P < .0001) and decreased FOXP3, CD25 and NFATC1 proteins (P < .0001). Active vitiligo (AV) patients showed reduced suppression of CD8⁺ & CD4⁺ T cells (P = .006, P = .015), increased IFN-γ (P = .036, P = .045), decreased IL-10 (P = .009, P = .021), FOXP3 (P = .0244) and NFATC1 (P = .019). Severe GV (50%-75% VASI) patients showed reduced suppression of CD8⁺ and CD4⁺ T cells (P = .0003, P = .001), increased IFN-γ (P = .0029, P < .0001), decreased IL-10 (P = .0057, P = .0017), FOXP3 (P = .002) and NFATC1 (P = .0347). VASI score was positively correlated with the suppression of CD8⁺ and CD4⁺ T cells (P = .0006, P < .0001), IL-10 (P = .0096, P = .029), FOXP3 (P = .0008) and NFATC1 (P = .043), whereas it was negatively correlated with IFN-γ (P = .0029, P = .0017). Early age of onset patients' Tregs demonstrated decreased suppression of CD8⁺ and CD4⁺ T cells (P = .0156, P = .0074), decreased TGF-β (P = .0212, P = .0083) and NFATC1 (P = .0103). NFATC1 was positively correlated with FOXP3 in Tregs (P < .0001). Our results suggest impaired Tregs suppressive function in GV patients due to decreased NFATC1, FOXP3, CD25, IL-10 and TGF-β resulting into increased CD8⁺ and CD4⁺ T-cell proliferation and IFN-γ production. For the first time, decreased NFATC1 levels were correlated with decreased FOXP3, thereby altering Treg cell function in GV patients. Additionally, decreased Treg cell function also affected onset, activity and severity of GV.     

银屑病外周血CD4+CD25+Foxp3+调节性T细胞的表达

目的: 检测CD4+CD25+Foxp3+调节性T细胞在不同类型银屑病患者中的表达.方法: 应用流式细胞仪检测外周血中CD4+CD25+Foxp3+调节性T细胞的表达.结果: 红皮病型银屑病患者外周血中CD4+CD25+Foxp3+调节性T细胞明显高于其他类型银屑病和正常对照组(P<0.05);斑块状银屑病CD4+CD25+Foxp3+T细胞比例高于点滴状患者(P<0.05);脓疱型银屑病患者中脓疱存在患者调节性T细胞比例明显低于脓疱消退患者(P<0.05).结论: CD4+CD25+Foxp3+调节性T细胞通过抑制效应T细胞在银屑病的病情活动中可能发挥重要作用.     

PI3K和Notch信号途径对寻常型银屑病患者外周血CD4+T细胞的增殖和活化发挥协同调控作用

 

目的 研究PI3K和Notch信号途径在寻常型银屑病患者外周静脉血CD4⁺ T细胞增殖、活化中的影响。方法 采集28例寻常型银屑病患者和28例健康对照外周静脉血,采用免疫磁珠法分选外周血CD4⁺ T细胞。将寻常型银屑病患者外周血CD4⁺ T细胞分为4组：空白对照组,10 μmol/L PI3K阻滞剂组（LY294002组）,25 μmol/L Notch阻滞剂组（DAPT组）,10 μmol/L LY294002+25 μmol/L DAPT组（LY294002+DAPT组）。均分别用植物血凝素（PHA）10 μg/mL和IL-2 1 000 U/mL刺激增殖6 h,采用FCM检测CD4⁺ T细胞内的CyclinA、Cyclin D1及P27^kipl细胞周期蛋白水平,逆转录-聚合酶链反应（RT-PCR）检测Cyclin A、Cyclin D1及P27^kipl mRNA水平,并对数据进行统计学处理。结果 CD4⁺ T细胞经免疫磁珠法分选后纯度为（90.00±3.90）％,CD4⁺ T细胞培养存活百分率达（92.50±4.60）％。寻常型银屑病患者外周血CD4⁺ T细胞Cyclin A、Cyclin D1水平分别为（27.60±3.80）％、（14.70±3.20）％,mRNA水平分别为0.56±0.14、1.37±0.39,与健康对照组（13.50±3.70）％、（7.80±2.00）％和（0.31±0.12）、（0.93±0.35）比较均明显升高,差异有统计学意义（P分别为0.002、0.037和0.008、0.043）。寻常型银屑病患者外周血CD4⁺ T细胞P27^kipl蛋白和mRNA分别为（23.50±3.60）％和（0.17±0.02）,均低于健康对照组的（36.80±5.60）％和（0.33±0.05）,差异有统计学意义（P分别为0.007、0.001）。与空白对照组CD4⁺ T细胞Cyclin D1蛋白和mRNA表达［分别为（12.30±3.50）％和（1.74±0..39）］比较,LY294002组、DAPT组、LY294002+DAPT组表达均下降,分别为（7.20±3.10）％、（8.20±2.50）％、（4.30±1.50）％和（1.11±0.29）、（1.26±0.28）、（0.63±0.20）,差异均有统计学意义（均P<0.05）。与空白对照组CD4⁺ T细胞P27^kipl蛋白［（21.80±3.20）％］比较,LY294002组、DAPT组、LY294002+DAPT组蛋白水平均升高,分别为（30.90±5.10）％、（27.60±5.20）％、（43.90±3.00）％,差异均有统计学意义（P分别为0.005、0.006、0.001）;与空白对照组CD4⁺ T细胞P27^kipl mRNA（0.15±0.08）比较,LY294002组、DAPT组、LY294002+DAPT组水平均上升,分别为（0.37±0.07）、（0.62±0.09）、（0.99±0.21）,差异均有统计学意义（P分别为0.018、0.002、0.003）。空白对照组、LY294002组、DAPT组、LY294002+DAPT组组间CD4⁺ T细胞Cyclin A蛋白和mRNA表达无显著性差异（均P>0.05）。结论 PI3K与Notch信号途径可协同增强CD4⁺ T细胞内正向调节蛋白Cyclin D1水平升高及负向调节蛋白P27^kipl水平下降,提示PI3K和Notch信号途径对寻常型银屑病患者外周血CD4⁺ T细胞的增殖、活化起着协同调控作用。

     

银屑病患者骨髓CD34~+细胞Hes-1基因的表达研究

目的:观察银屑病患者骨髓CD34~+细胞Hes-1基因的表达.方法:以β-肌动蛋白为内参照,采用反转录(RT)-PCR法半定量检测24例银屑病患者及18名正常人骨髓CD34~+细胞Hes-1 mRNA的表达水平.结果:与正常对照组相比,银屑病患者组Hes-1mRNA表达水平明显升高,二者差别有统计学意义.结论:造血细胞发育过程中重要的转录因子Hes-1的高表达可能与银屑病患者骨髓造血细胞的增殖活性异常有关.     

白塞病患者外周血CD4+CD25+调节性T细胞的检测及其临床意义

目的检测白塞病(BD)患者外周血Cd4+ CD25+调节性T细胞数量变化并分析其与疾病活动性的关系,探讨其临床意义.方法利用流式细胞仪和单克隆荧光抗体技术测定31例BD患者和27例健康对照者外周血中CD4+CD25+调节性T细胞在CD3+Cd4+细胞中的比例.结果活动期患者外周血中CD4+CD25+调节性T细胞在CD3+CD4+细胞中的百分率(6.43%±2.54%),低于健康对照者(8.17%±2.87%)(P＜0.05).非活动期患者外周血中CD4+CD25+调节性T细胞在CD3+ CD4+细胞中的百分率(8.35%±2.31%),略高于健康对照者(P＞0.05).结论BD患者外周血中CD4+CD25+调节性T细胞在CD3+CD4+细胞中的比例降低与疾病活动相关.通过检测外周血CD4+CD25+调节性T细胞在CD3+ CD4+细胞中的比例来评估机体免疫状态是一个可行的办法.     

斑秃患者外周血CD4+CD25+Foxp3调节性T细胞及T淋巴细胞亚群的测定

目的 研究斑秃患者外周血中CD4+CD25+调节性T细胞数量及CD4+、CD8+ T淋巴细胞亚群数量与斑秃疾病严重程度的关系。方法 对斑秃进行病情分组，以流式细胞仪检测17例重度、15例局限型斑秃患者和25例正常人对照者外周血中有功能活性的CD4+CD25+调节性T细胞（即CD4+CD25+ Foxp 3 T 细胞）在CD4+ T淋巴细胞中的比率，CD4+和CD8+占T淋巴细胞的比率。 结果 重度斑秃患者外周血中有功能活性的CD4+CD25+ Foxp 3 T细胞占CD4+ T细胞比率为0.54% ± 0.31%，显著低于正常人对照组（3.21% ± 0.76%）及局限型斑秃患者（2.71% ± 0.37%，P ＜ 0.001）；与正常人对照组比较，差异无统计学意义（P ＞ 0.05）。重度斑秃患者的CD4+占T淋巴细胞的比率为32.61% ± 3.48%，显著低于正常人对照组（43.0% ± 3.63%，P ＜ 0.001），而CD8+占T淋巴细胞的比率为40.96% ± 8.54%，显著高于正常人对照组（25.23% ± 2.14%，P ＜ 0.001）。局限型斑秃患者的此两项指标分别为41.25% ± 4.27%和26.6% ± 2.28%，与对照组差异无统计学意义（P ＞ 0.05）。重度斑秃患者的CD8+占T淋巴细胞的比率与CD4+CD25+ Foxp 3调节性 T 细胞占CD4+ T细胞的比率有负相关关系（r ＝ －0.94，P ＜ 0.001）。结论 重度斑秃可能与外周血中CD4+CD25+ T细胞数量的减少和功能活性的降低有关。     

CD4~+CD25~+调节性T细胞与Th17细胞在寻常型银屑病中的表达

目的:检测外周血中CD4~+CD25~+调节性T细胞(简称Treg细胞)与Th17细胞在寻常型银屑病(PV)中的表达。方法:34例寻常型银屑病患者,18例正常人作为对照。采用流式细胞术检测外周血中Treg细胞、FOXP3~+Treg细胞及Th17细胞的表达水平。结果:PV患者外周血中Treg细胞比例和FOXP3~+Treg细胞比例分别为(3.68±1.22)%和(0.53±0.19)%,低于正常对照组的(6.63±1.00)%和(0.76±0.14)%(P0.05)。Th17细胞比例为(2.20±0.78)%,高于正常对照组的(0.65±0.22)%(P0.05)。PV患者外周血中Treg细胞的表达与FOXP3~+Treg细胞的表达呈正相关(r=0.563,P0.05),而Treg细胞的表达与Th17细胞的表达呈负相关(r=-0.522,P0.05);Treg细胞和Th17细胞二者与PASI评分无相关性,与病程亦无相关性。结论:Treg细胞表达的减少及Th17细胞应答的增强,可能是导致PV免疫失衡的重要原因。     

Regulation of nickel-induced T-cell responsiveness by CD4+CD25+ cells in contact allergic patients and healthy individuals

In this study, we investigated the capacity of CD4⁺CD25⁺ regulatory T cells to suppress nickel‐specific effector T cells, both in nickel‐allergic patients and healthy controls. CD4⁺ cells isolated from allergic patients showed an increased proliferative response to nickel, whereas CD4⁺ cells from negative controls did not respond to allergen. When CD4⁺CD25⁺ cells were depleted, nickel‐specific responsiveness was strongly increased both in allergic and in non‐allergic individuals, with the most pronounced effect in allergic patients. These regulatory T cells were anergic to nickel but inhibited nickel‐specific CD4⁺CD25^– effector T cells in coculture experiments. CD4⁺CD25⁺ cells from nickel‐allergic patients showed only a limited capacity to suppress effector T‐cell responsiveness, because an increased nickel reactivity could still be detected in these cocultures. None of the isolated CD4⁺CD25⁺ cells, either isolated from healthy controls or allergic patients, produced IL‐10 in response to nickel. Overall, these results support the view that CD4⁺CD25⁺ cells can control the activation of nickel‐specific effector T cells in non‐allergic individuals, whereas this regulatory capacity is impaired in allergic patients. To investigate the presence of allergen‐specific regulatory T cells in truly naïve, non‐sensitized individuals, T‐cell reactivity should also be studied with non‐environmental contact allergens, such as para‐phenylenediamine.