CD4^＋T淋巴细胞表面CD4^＋CD45RA和CD4^＋CD45RO在支气管哮喘患儿外周血中的表达

目的探讨CD4^＋CD45RA和CD4^＋CD45RO分子在支气管哮喘患儿中的表达及其意义。方法分别收集支气管哮喘发作期28例、支气管哮喘缓解期27例、健康对照儿童20例抗凝静脉血100μL，采用异硫氰酸荧光素（FITC）标记的抗CIM单抗、藻红蛋白（PE）标记的抗CD45RA单抗和PE-菁蓝色素荧光素（PE—Cy5）标记的抗CD45RO单抗，流式细胞仪检测各组儿童外周血CD4^＋T淋巴细胞表面CD45RA和CD45RO的表达。采用SPSS13．0软件进行统计学分析。结果与健康对照和支气管哮喘缓解组患儿比较，支气管哮喘发作组患儿CD4^＋CD45RA^＋T细胞明显减少（q=12．47，8，39Pa〈0．05），CD4^＋CD45RO^＋T细胞显著升高（q=9．50，8．30Pa〈0．05），CD4^＋CD45RA^＋／CD4^＋CD45RO^＋细胞比值显著降低（q=8．96，6．21P。〈0．05）；支气管哮喘缓解组患儿CD4^＋CD45RA^＋T细胞较健康对照组明显升高（q=3．08P〈0．05），CD4^＋CD45RO^＋T细胞及CD4^＋CD45RA^＋／CD4^＋CD45RO^＋细胞比值与健康对照组比较差异无显著性（q=0．45，2．02Pa〉0．05）。结论外周血CD4^＋CD45RA^＋和CD4^＋CD45RO^＋T淋巴细胞平衡失调可能参与支气管哮喘的发病。     

静脉免疫球蛋白对新生儿脐血淋巴细胞TGF-β1和IL-10分泌的影响

目的从IL-10和TGF-β1分泌的角度研究IVIG对新生儿淋巴细胞免疫功能的调节作用。方法应用IVIG和PHA不同组合对脐带血单个核细胞(cord blood mononuclear cell,CBMC)或CD3 T淋巴细胞进行刺激培养;应用ELISA法检测细胞IL-10和TGF-β1的分泌,并与成人外周血单个核细胞比较。结果IVIG可抑制PHA诱导的新生儿CBMC IL-10和TGF-β1的分泌。IVIG对新生儿CBMC IL-10和TGF-β1分泌的抑制作用与细胞是否被活化无关。IVIG对脐带血CD3 T淋巴细胞IL-10分泌的抑制作用明显低于新生儿CBMC,对脐带血CD3 T淋巴细胞TGF-β1分泌无明显影响。结论IVIG对淋巴细胞的免疫抑制并非通过诱导抑制性细胞因子分泌发挥作用,可能通过直接作用于淋巴细胞或通过其他间接机制而起作用。IVIG对IL-10和TGF-β1分泌的影响可能因所作用的细胞类型和细胞所处的状态不同而不同,因此应在充分了解新生儿免疫状态的基础上合理使用IVIG。     

溴隐亭对植物血凝素诱导活化T淋巴细胞的影响

目的 研究溴隐亭(BRC)对植物血凝素(PHA)诱导活化T淋巴细胞的影响.方法 用泌乳素(PRL)与BBC单独和联合刺激培养PHA诱导活化的CD4 T淋巴细胞系Jurkat E6-1细胞,利用实时聚合酶链反应(RT-PCR)技术检测活化T淋巴细胞重要信号分子转接蛋白(LAT)、T细胞受体相关的相对分子质量为70000的蛋白激酶ζ链(ZAP-70)mRNA表达变化情况;利用Real time-PCR方法检测活化T淋巴细胞自身PRL mRNA表达变化情况;利用流式细胞术检测T淋巴细胞活化早期表面标志细胞分化抗原CD25分子表达变化情况;利用脂质体转染荧光素酶报告系统检测T淋巴细胞活化的核转录因子-kB(NF-kB)活性变化情况.结果 1.BRC可抑制PHA诱导的T淋巴细胞活化和PRL-泌乳素受体(PRLR)信号转导途径的共同信号分子ZAP-70 mRNA及活化T淋巴细胞自身PRL mRNA的表达;2.BRC促进了活化T淋巴细胞信号分子LAT mRNA和活化T淋巴细胞表面CD25分子的表达;3.BRC抑制了PHA诱导的活化T淋巴细胞核NF-kB活性.结论 BRC可通过抑制T淋巴细胞活化和PRL-PRLR途径中的共同信号分子ZAP-70及活化T淋巴细胞自身PRL mRNA分泌,对T淋巴细胞活化发挥抑制作用.     

幼年特发性关节炎患儿外周血Th细胞亚群变化

目的探讨幼年特发性关节炎(JIA)患儿外周血CD4 T淋巴细胞及其亚群CD4 CD45RA 、CD4 CD45RO 的表达及其临床意义。方法采用免疫荧光标记技术和流式细胞仪检测36例JIA患儿外周血CD4 T淋巴细胞及其亚群CD4 CD45RA 、CD4 CD45RO 的表达,同期检测20例年龄、性别无差异的健康儿童为对照。结果JIA患儿外周血CD4 T淋巴细胞明显低于对照组(t=2.099,P<0.05),CD4 CD45RA T淋巴细胞数与对照组比较明显降低(t=3.450,P<0.01),CD4 CD45RO T淋巴细胞数明显升高(t=3.913,P<0.01),CD4 CD45RA T/CD4 CD45RO T比值明显降低(t=4.904,P<0.01);与对照组比较,JIA各亚型(全身型、多关节型、少关节型)的CD4 CD45RO T淋巴细胞数均明显升高,CD4 CD45RA T/CD4 CD45RO T比值明显降低(P<0.01);CD4 CD45RA T淋巴细胞数与正常对照组比较在全身型中显著降低(t=4.192,P<0.01);在多关节型中明显降低(t=2.214,P<0.05);在少关节型中稍有降低,但与对照组比较差异无显著性(t=1.793,P>0.05)。结论JIA患儿的免疫功能紊乱主要表现为CD4 T淋巴细胞及其亚群CD4 CD45RA T/CD4 CD45RO T失衡,这可能在JIA发病机制中起着重要的作用。     

D4+T淋巴细胞表面CD4+CD45RA和CD4+CD45RO在支气管哮喘患儿外周血中的表达

目的 探讨CD4 CD45RA和CD4 CD45RO分子在支气管哮喘患儿中的表达及其意义.方法 分别收集支气管哮喘发作期28例、支气管哮喘缓解期27例、健康对照儿童20例抗凝静脉血100μL,采用异硫氰酸荧光素(FITC)标记的抗CD4单抗、藻红蛋白(PE)标记的抗CD45RA单抗和PE-菁蓝色素荧光素(PE-Cy5)标记的抗CD45RO单抗,流式细胞仪检测各组儿童外周血CD4T淋巴细胞表面CD45RA和CD45RO的表达.采用SPSS13.0软件进行统计学分析.结果 与健康对照和支气管哮喘缓解组患儿比较,支气管哮喘发作组患儿CD4 CD45RA T细胞明显减少(q=12.47,8.39 Pa<0.05),CD4 CD45RO T细胞显著升高(q=9.50,8.30 Pa<0.05),CD4 CD45RA /CD4 CD45RO 细胞比值显著降低(q=8.96,6.21 Pa<0.05);支气管哮喘缓解组患儿CD4 CD45RA T细胞较健康对照组明显升高(q=3.08 P<0.05),CD4 CD45RO T细胞及CD4 CD45RA /CD4 CD45RO 细胞比值与健康对照组比较差异无显著性(q=0.45,2.02 Pa>0.05).结论 外周血CD4 CD45RA 和CD4 CD45RO T淋巴细胞平衡失调可能参与支气管哮喘的发病.     

幼年类风湿关节炎患儿血清白介素-15变化与T_H细胞亚群表达的研究

目的：探讨幼年类风湿关节炎(JRA)患儿血清白介素15变化及其TH细胞亚群CD4+CD45RA+,CD4+CD45RO+的表达变化。方法：采用ELISA方法检测39例JRA患儿的血清IL15的水平,并同期选择26例年龄、性别无差异的健康儿童为对照。对其中24例JRA患儿采用免疫荧光标记技术和流式细胞仪检测外周血CD4+T淋巴细胞亚群CD4+CD45RA+,CD4+CD45RO+的表达。结果：JRA患儿组血清IL15水平显著高于正常对照组(P<0.05);JRA常见亚型中全身型患儿血清IL15水平明显升高,与对照组比较差异有显著性(P<0.01),而少关节型、多关节型患儿IL15水平与对照组比较差异无显著性(P>0.05);治疗后IL15水平较治疗前明显下降(P<0.01);JRA患儿血清IL15水平与外周血白细胞计数呈正相关(r=0.347,P<0.05),与血沉无相关(r=0.307,P>0.05),与C反应蛋白呈显著正相关(r=0.452,P<0.01);IL15高表达组患儿外周血CD4+CD45RO+T淋巴细胞数明显高于IL15低表达组患儿(P<0.05),CD4+CD45RA+T淋巴细胞数、CD4+CD45RA+T/CD4+CD45RO+T比值略低于IL15低表达组患儿,差异无显著性(P>0.05)。结论：JRA患儿血清IL15的水平显著升高;IL15升高使JRA患儿外周血CD4+T细胞表面CD45RA分子向CD45RO分子转换,促使T淋巴细胞大量激活,进而介导组织免疫病理损伤;在临床上可通过检测IL15以判断JRA的病情状况,为JRA治疗提供理论依据。     

人脐血T、B淋巴细胞和NK细胞的免疫学表达特性

目的 探讨人脐血T、B淋巴细胞和NK细胞，以及T／NK细胞杀伤性抑制性受体（KIR）表达的免疫学特性及其意义。方法 应用流式细胞仪检测26例正常新生儿脐血的T、B淋巴细胞和NK细胞抗原标记，包括CD45RA、CD45RO、CD69、CD25、CD40L、CD40、CD10、CD20和CD16等抗原的表达，以及脐血T／NK细胞上KIR分子（CD158a和CD158b抗原）的表达，并与正常儿童外周血比较。结果 脐血T淋巴细胞中CD45RA^ 细胞表达高于外周血（P＜0．01），CD45RO^ 则明显低于外周血（P＜0．01）；脐血T细胞CD69表达极低；CD25在CD8^ 细胞亚群中几乎不表达；CD40L在脐血T细胞中表达低于外周血（P＜0．05）。脐血B淋巴细胞中不成熟亚群CD10^ ／CD19^ 比例增高，成熟B细胞表型CD19、CD20、CD40等抗原均明显高于正常外周血（P＜0．01）。脐血中T淋巴细胞和NK细胞均存在KIR分子表达；脐血和外周血中T淋巴细胞CD158分子表达低于NK细胞（P＜0．01），脐血T淋巴细胞亚群中CD158分子表达低于正常外周血；CD158几乎不表达于CD4^ T细胞，主要表达于CD8^ T细胞，且以CD158a^ 为主；脐血中NK细胞CD158分子表达高于T淋巴细胞（P＜0．05），但明显低于外周血NK细胞KIR的表达（P＜0．01）。结论 脐血T淋巴细胞包括原始和早期T细胞以及T细胞受体表达障碍，导致脐血T淋巴细胞免疫功能不成熟，可能是脐血移植（UCBT）后移植物抗宿主病（GVHD）发生率低和程度轻的重要原因之一。脐血B淋巴细胞免疫应答障碍可能缘于T淋巴细胞表型或功能的障碍。脐血T／NK细胞KIR的表达特性提示，KIR可能与UCBT中GVHD和移植物抗白血病（GVL）效应有关。     

sCD40L、CD4＋CD45RA＋T细胞及CD4＋CD45RO＋T细胞在儿童ITP中的作用

目的探讨协同刺激分子可溶性CD40配体（sCD40L）及CD4＋T辅助细胞CD45RA和CD45RO亚群在儿童特发性血小板减少性紫癜中的变化。方法用ELISA法检测25例ITP患儿血浆sCD40L水平;用微量全血流式细胞术法检测ITP患儿外周血CD4＋T辅助细胞CD45RA和CD45RO的表达率;并对sCD40L与血小板计数进行相关分析。结果ITP患儿血浆sCD40L浓度明显升高,与对照组比较差异有显著性（P〈0.05）;CITP组血浆sCD40L浓度升高更为明显,与AITP组或对照组比较差异均有显著性（P〈0.05）。ITP患儿CD4＋CD45RA＋T细胞表达率下降,CD4＋CD45RO＋T细胞表达率升高,差异均有显著性意义（P〈0.05）,而AITP和CITP之间差异无显著性（P〉0.05）。血浆sCD40L与外周血小板计数无相关性（r=-0.047,P〉0.05）。结论CD40L高表达导致的CD40L/CD40信号传导通路异常可能参与ITP发病;ITP患儿存在Th细胞亚群偏移,表现为Th1细胞减少,Th2细胞增多。     

RSV感染患儿外周血CD_4~*”CD_(45)RO~+CD_(45)RA~+表达变化的研究

目的：探讨下呼吸道感染呼吸道合胞病毒(RSV)患儿外周血辅助性T淋巴细胞(CD4),原始T细胞(CD45RA+),记忆性T细胞(CD45RO+)表达的变化。方法：用单克隆抗体免疫荧光标记,流式细胞仪检测30例RSV下呼吸道感染患儿急性期外周血单个核细胞(PBMCs)CD4+,CD45RA+细胞,其中11例同时检测CD45RO+细胞,同期检测9例年龄、性别无差异的健康儿为对照。结果：RSV下呼吸道感染组患儿CD4为(32.74±10.60)%,明显低于对照组(40.76±6.82)%,2组有显著性差异(P0.05)。结论：RSV感染急性期存在免疫功能紊乱,外周血CD4,CD45RO+下降,而CD45RA+明显增加,这可能是CD45RO+向呼吸道迁移的结果。     

sCD40L、CD4~+CD45RA~+T细胞及CD4~+CD45RO~+T细胞在儿童ITP中的作用

目的探讨协同刺激分子可溶性CD40配体(sCD40L)及CD4+T辅助细胞CD45RA和CD45RO亚群在儿童特发性血小板减少性紫癜中的变化。方法用ELISA法检测25例ITP患儿血浆sCD40L水平;用微量全血流式细胞术法检测ITP患儿外周血CD4+T辅助细胞CD45RA和CD45RO的表达率;并对sCD40L与血小板计数进行相关分析。结果ITP患儿血浆sCD40L浓度明显升高,与对照组比较差异有显著性(P<0.05);CITP组血浆sCD40L浓度升高更为明显,与AITP组或对照组比较差异均有显著性(P<0.05)。ITP患儿CD4+CD45RA+T细胞表达率下降,CD4+CD45RO+T细胞表达率升高,差异均有显著性意义(P<0.05),而AITP和CITP之间差异无显著性(P>0.05)。血浆sCD40L与外周血小板计数无相关性(r=-0.047,P>0.05)。结论CD40L高表达导致的CD40L/CD40信号传导通路异常可能参与ITP发病;ITP患儿存在Th细胞亚群偏移,表现为Th1细胞减少,Th2细胞增多。     

Transient decrease in the CD45RA expression on T lymphocytes in neonates with fetal distress

To determine the expression of CD45 isoforms on T lymphocytes in neonates with fetal distress and to evaluate its diagnostic accuracy, peripheral blood samples were examined in 53 neonates who were classified into one of three groups: group I: 'control' group (n = 23), group II: 'mild distress' group (n = 15), and group III: 'moderate distress' group (n = 15). The expression of CD3 (mean +/- SD 24.2 +/- 10.1%), CD4 (23.0 +/- 5.7%), and CD45RA (27.3 +/- 9.6%) on total lymphocytes and the expression of CD45RA on CD4+ T lymphocytes (13.7 +/- 4.7%) in group III were significantly lower than in the other two groups 0-3 days after birth. Sensitivity and specificity of the CD45RA expression on CD4+ T lymphocytes for discrimination of group III were calculated as 0.79 and 1.0, respectively, when the cutoff value was 22.7%. The low CD3, CD4, and CD45RA expression returned to normal levels 10 days and more after birth. There were no differences in the CD8 and CD45RO expression between the groups. We conclude that CD4+ T lymphocytes from neonates with fetal distress show a transient decrease in the CD45RA expression without an increase in the CD45RO expression, and, therefore, analysis of the CD45 isoform expression is useful for laboratory evaluation of fetal distress.     

Effect of interleukin-7 and -15 on activation of purified umbilical cord blood and adult peripheral blood CD4+ T cells

We investigated the effect of two IL-2 receptor gamma chain (IL-2R-gammac)-signaling cytokines, IL-7 and IL-15, on the activation of purified CD4+ lymphocytes from umbilical cord blood (CB) and adult peripheral blood (APB) by assessing the expression of the IL-2 receptor-alpha (CD25) and Fas (CD95) on CD45RA+ (na?ve) and CD45RO+ (memory) CD4+ subsets. Induced CD40L (CD154) expression following phorbol 12-myristate 13-acetate and ionomycin (P+I) stimulation was also examined on cultured CB CD4+ cells. Incubation with IL-15 at 10 ng/ml resulted in a significant increase in the mean fluorescence intensity (MFI) of CD25 on CB CD4+/CD45RA+ cells (exceeding those of APB) without affecting the percentage of CD25-expressing CD45RA+ cells (%CD25/CD45RA). In contrast, both CD25 MFI and %CD25/CD45RA were enhanced on IL-15-treated APB CD4+ cells. CD95 expression (both percent expression and MFI) on CB CD4+/CD45RA+ cells were also enhanced by IL-15, but to a lesser extent compared to the response of ABP. IL-7, used at a concentration equivalent to IL-15, had little effect on APB CD25/CD95 and CB CD25 expression, but did enhance %CD95 expression on CB CD4+/CD45RA+ cells. Both IL-7 and IL-15 could augment the P+I-induced CD40L expression on CB CD4+/CD45RA+ T cells. However, the enhancing effect of IL-15 on CB CD40L/CD45RA expression was more sustained than that of IL-7. Thus, our study demonstrated differential activation of CB CD4+/CD45RA+ cells in response to IL-7 and IL-15 compared to adult counterparts, and the different T-enhancing function between IL-15 and IL-7.     

肺炎支原体感染患儿T淋巴细胞亚群检测及分析

目的　观察肺炎支原体肺炎患儿急性期外周血T淋巴细胞亚群、T淋巴细胞活化状态的改变,探讨其发病机制。方法　采用流式细胞仪技术检测了2 0 0 2年1 0月至2 0 0 3年6月就诊于上海市金山区中心医院的1 7例肺炎支原体肺炎患儿急性期外周血T淋巴细胞亚群及T细胞亚群上CD2 5+的表达和CD4+细胞上CD4+CD45RA+、CD4+CD45RO+的表达;对照组为1 0例健康体检儿童。两组年龄、性别差异无显著意义。结果　肺炎支原体肺炎患儿急性期外周血CD3 +百分率( % )为( 62 . 2 3±6 .2 7) ,较对照组( 68 .60±4. 74)低,差异有显著性意义(P <0 . 0 5) ;CD4+、CD8+百分率较对照组差异无显著性意义(P >0. 0 5) ;CD8+CD2 5+百分率( % )为( 0 . 61±0 . 58) ,较对照组( 2 .1 6±0 . 40 )降低,差异有极显著性意义(P <0 .0 1 ) ;CD4+CD45RA+/CD4+CD45RO+比值与对照组相比降低(P <0 . 0 5)。结论　肺炎支原体肺炎时存在细胞免疫失调,主要表现为总T细胞降低,T细胞活化障碍和CD4+CD45RA+/CD4+CD45RO+平衡失调。     

CD95 (APO-1/Fas) expression on naive CD4(+) T cells increases with disease progression in HIV-infected children and adolescents: effect of highly active antiretroviral therapy (HAART)

We studied the expression of the CD95 receptor (APO-1/Fas) on peripheral blood T cell subpopulations in 37 HIV-1-infected children and adolescents stratified according to disease stage or antiretroviral treatment regimen and compared the results to values obtained in 12 healthy age-matched control subjects. CD95 expression on CD45RA(+) CD45RO(-)/CD62L(+) (resting/naive) and CD45RO(+) CD45RA(-) (primed/memory) CD4(+) and CD8(+) T cells was assessed quantitatively by four-color and three-color flow cytometry. CD4(+) T cells contained a population of predominantly CD95(-) resting/naive cells and a population of CD95(high) primed/memory cells, whereas CD8(+) T cells had a more uniform pattern of CD95 expression. The percentage of CD95(+) CD4(+) T cells increased with disease progression because of both an augmented median fluorescence intensity on resting/na?ve cells and an increased percentage of CD95(high) cells. Patients with highly active antiretroviral combination therapy who maintained stable CD4 counts in the presence of elevated plasma viral load had nearly normal numbers of CD95(-) resting/naive CD4(+) T cells, whereas CD95 expression in the CD8(+) T cell subset was still elevated compared with control subjects. Low CD95 expression on resting/naive CD4(+) T cells may therefore indicate a low risk for disease progression in antiretrovirally treated and untreated patients.     

Acute chylothorax in children: selective retention of memory T cells and natural killer cells

OBJECTIVE: To assess for immunodeficiency in patients with hypogammaglobulinemia in the setting of draining acute chylothorax. STUDY DESIGN: Humoral and cellular immunity was evaluated in 8 patients with chylothorax. Chylous fluid was also analyzed to document cellular losses. Data regarding clinical course and immunologic characteristics were reviewed retrospectively. RESULTS: All patients had hypogammaglobulinemia (IgG=179+/-35 mg/dL) as well as lymphopenia (985+/-636 cells/mm(3)). T cells were decreased and natural killer cells increased in peripheral blood. The converse was found in chylous fluid. The ratio of CD3+/CD45RA+ naive: CD3+/CD45RO+ memory T cells was greater in chyle than in peripheral blood. In vitro proliferative responses to antigens and mitogens were similar to control subjects, and previously immunized patients maintained evidence of protective vaccine-specific humoral immunity. To treat hypogammaglobulinemia, patients received intravenous immunoglobulin (IVIG) to maintain IgG within normal range; 6 of 8 patients had serious infections before receiving IVIG compared with 4 of 8 patients during the period of IVIG administration. CONCLUSION: Draining chylothorax resulted in IgG and lymphocyte depletion with preferential retention of memory T cells and natural killer cells in the circulation. Overall, protective-specific antibody levels and T cell function were maintained. IVIG administration did not lead to discernible protection from infectious complications in this small group of patients.     

Analysis of changes in the percentage of B (CD19) and T (CD3) lymphocytes,subsets CD4, CD8 and their memory (CD45RO), and naive (CD45RA) T cells in children with immune and non-immune thyroid diseases

Graves' disease (GD) is an autoimmune thyroid disease caused by immunological abnormality. The immune cells (lymphocytes T and B) which infiltrate the thyroid gland play a key role in the development of autoimmune thyroid disease (AITD). The aim of this study was to evaluate the differences between distribution of T (CD3) lymphocytes, subsets CD4, CD8, and their memory (CD45RO), and naive (CD45RA) T cells and B (CD19) lymphocytes in the peripheral blood of patients with Graves' disease (GD) (n = 33, mean age 15.9 +/- 5.9 years) and non-toxic nodular goiter (NTNG) (n = 25, mean age 15.2 years), in comparison to age- and sexmatched healthy control subjects (n = 25, mean age 15.9 years). The percentages of peripheral blood lymphocyte subsets were analyzed by three-color flow cytometry using a Coulter EPICS XL cytometer. In the untreated Graves' patients we observed an increase in the percentage of CD19+ (p<0.007, p<0.003), CD4+ (p<0.004, p<0.017), CD4+CD45RO+ (p<0.04, NS), CD4/CD8 ratio (p<0.002, p<0.001) and a decrease in the percentage of CD8+ (p<0.02, p<0.02), CD4+CD45RA+ (p<0.04, p<0.03) cells in comparison to the healthy control subjects and euthyroid Graves' patients. These abnormalities were absent in children with non-toxic nodular goiter. In addition, the levels of CD3+, CD4+CD8+, CD8+CD45RO+ T cells and CD8 lymphocytes co-expressing CD45RA and CD45RO antigens were similar in all groups and no statistically significant differences were found in comparison to the healthy controls. In the untreated Graves' patients we found a positive correlation between serum levels of fT4 and fT3 and the percentage of CD19+ lymphocytes (r = 0.45, p<0.01, r = 0.37, p<0.04), between serum level of fT4 and the percentage of CD4CD45RO (r = 0.4, p<0.02) lymphocytes and between concentration of TRAb and CD4+ (r = 0.38, p <0.04) and CD19+ (r = 0.39, p<0.016) cells. Statistically significant negative correlations existed between TRAb, TPO-Ab or TG-Ab concentration in blood serum and the percentage of CD8+ lymphocytes (r = -0.55, p<0.002; r = -0.41, p<0.02; r = -0.51, p<0.004), and between fT4 concentration and the percentage of CD8+ (r = -0.39, p<0.02) lymphocytes. No such correlation was detected in patients with non-toxic nodular goiter. We conclude that the abnormal distribution of B lymphocytes, memory and naive T cell subsets in the peripheral blood in children and adolescents with untreated Graves' disease suggests their role in the development of autoimmunity. The normalization in the percentage of these immune cells after thyrostatic treatment in comparison to newly diagnosed patients confirms the immunomodulatory effect of methimazole therapy.     

Immunoreconstitution after ritonavir therapy in children with human immunodeficiency virus infection involves multiple lymphocyte lineages

OBJECTIVE: To evaluate lymphocyte reconstitution after protease inhibitor therapy in children with human immunodeficiency virus (HIV) infection. STUDY DESIGN: Forty-four HIV-infected children receiving ritonavir monotherapy followed by the addition of zidovudine and didanosine were evaluated during a phase I/II clinical trial. The cohort had a median age of 6.8 years and advanced disease (57% Centers for Disease Control and Prevention stage C, 73% immune stage 3) and was naive to protease inhibitor therapy. RESULTS: After 4 weeks of therapy, there was a significant increase in CD4(+) and CD8(+) T cells. CD4(+) T cells continued to increase, whereas CD8(+) T cells returned to baseline by 24 weeks. Unexpectedly, there was a significant increase in B cells. Changes in CD4(+) T-cell subsets revealed an initial increase in CD4(+) CD45RO T cells followed by a sustained increase in CD4(+) CD45RA T cells. Children <6 years of age had the highest increase in all lymphocyte populations. Significant improvement in CD4(+) T-cell counts was observed even in those children whose viral burden returned to pre-therapy levels. CONCLUSIONS: Early increases in lymphocytes after ritonavir therapy are a result of recirculation, as shown by increases in B cells and CD4(+) CD45RO and CD8(+) T cells. Children exhibited a high potential to reconstitute CD4(+) CD45RA T cells even with advanced disease and incomplete viral suppression.     

幽门螺杆菌感染儿童胃窦黏膜CD4+、CD8+的研究

目的研究幽门螺杆菌(Hp)感染儿童胃窦黏膜T淋巴细胞CD4+、CD8+ 及CD4+/CD8+的变化.方法流式细胞仪(FCM)直接免疫荧光法测定79例慢性浅表性胃炎(CSG)患儿(Hp+44例,Hp-35例)胃窦黏膜及其中33例(Hp+12例,Hp-21例)患儿外周血的T淋巴细胞CD4+、CD8+变化.所有患儿均行内镜检查并取胃窦黏膜作快速尿素酶试验、组织病理学检查及胃窦黏膜单个核细胞提取.33例儿童同时抽取外周静脉血2 ml.提取的胃窦黏膜及外周血单个核细胞经异硫氰酸荧光素标记CD3(CD3-FITC)、藻红蛋白标记CD4(CD4-PE)、多甲藻(黄)素叶绿素蛋白标记CD8(CD8-PerCP)单克隆抗体染色后行流式细胞术测定,其中胃窦黏膜T淋巴细胞的检测以CD3设门.结果 (1)胃窦黏膜CD3+细胞的检出率分别为Hp-CSG组(3.26±1.98)%,Hp+CSG组(4.37±1.97)%.(2)胃窦黏膜CD3+细胞中CD4+,CD8+的相对百分比及CD4+/CD8+值分别为Hp-CSG组为(23.74±10.37)%,(47.04±12.00)%,0.52±0.23,Hp+CSG组为(40.28±11.35)%,(27.91±8.84)%,1.55±0.52.Hp+CSG组胃窦黏膜CD4+细胞相对百分比、CD4+/CD8+比值明显高于Hp-CSG组,CD8+细胞相对百分比则低于Hp-CSG组(P均<0.01).(3)两组外周血T淋巴细胞CD3+(%)、CD4+(%)、CD8+(%)、CD4+/CD8+的比较差异无统计学意义.结论儿童Hp+CSG的T淋巴细胞变化为局部胃窦黏膜的细胞免疫应答所致.