流式细胞术检测拉米夫定对慢性乙型肝炎患者T细胞亚群的影响

目的研究拉米夫定对慢性乙型肝炎（CHB）患者细胞免疫功能的影响.方法采用流式细胞术检测50例CHB患者在服用拉米夫定前后外周血T细胞亚群,同时检测45例健康体检者外周血T细胞亚群作为对照.结果CHB患者在使用拉米夫定后,CD4 T细胞百分比较使用前明显升高（P〈0.05）,CD8 T细胞百分比明显下降（P〈0.05）,CD4/CD8明显升高（P〈0.05）.结论拉米夫定可改善CHB患者的细胞免疫功能.     

肝癌患者手术前后T细胞亚群的变化特点及其意义

目的:探讨肝癌患者手术前后外周血T淋巴细胞亚群的变化特点.方法:应用APAAP法测定30例肝癌患者手术前后的CD3、CD4和CD8细胞的阳性细胞百分率及其比值,并与正常对照组比较分析.结果:30例肝癌患者手术前CD3,CD4及CD4/CD8比值明显低于正常对照组,差异有显著性(P＜0.01),手术后CD4/CD8的比值有明显提高,差异也有显著性(P＜0.01),提示肝癌患者手术前后CD4/CD8比值有显著改变.结论:监测外周血CD4/CD8的比值可作为评价肝癌患者病情及手术后预后的一个参考指标.     

慢性乙型肝炎患者外周血CD45RA+,CD45RO+T淋巴细胞亚群的特点及临床意义

目的探讨慢性乙型肝炎患者外周血CD4 CD45RA ,CD4 CD45RO ,CD8 CD45RA 和CD8 CD45RO T淋巴细胞亚群的特点及其与肝病病情的关系.方法采集46例轻中度慢性乙型肝炎患者、58例重度慢性乙型肝炎患者和30例健康人的外周抗凝血,应用流式细胞技术三色荧光分析法对其外周血中CD4 CD45RA ,CD4 CD45RO ,CD8 CD45RA 和CD8 CD45RO T淋巴细胞亚群进行检测.结果轻中、重度慢性乙型肝炎患者与正常人相比,其外周血中CD4 ,CD8 T细胞均无明显改变;CD8 CD45RA T细胞均明显降低,CD8 CD45RO T细胞均明显增高,而CD4 CD45RA ,CD4 CD45RO T细胞均无明显改变;重度慢性乙型肝炎患者与轻中度慢性乙型肝炎患者相比,CD8 CD45RA T细胞明显降低(P<0.05),CD8 CD45RO T细胞明显升高(P<0.05).结论乙型肝炎慢性化过程中,CD8 CD45RO T细胞起重要作用且与慢性乙型肝炎患者病情的进展呈正相关;检测CD4 CD45RA ,CD4 CD45RO ,CD8 CD45RA 和CD8 CD45RO T淋巴细胞亚群比检测CD4 和CD8 T细胞亚群能使我们更加正确、充分、全面地了解慢性乙型肝炎的发病机制和预后,从而有效地指导临床治疗.     

IFN-α治疗对慢性丙型肝炎患者CD8~+T细胞亚群Tim-3表达水平的影响

为探讨应用IFN-α治疗和未治疗的慢性丙型肝炎患者外周血CD8+T细胞亚群细胞频数及各亚群上Tim-3表达的变化。采用流式细胞术检测IFN-α治疗和未治疗的慢丙肝患者外周血中CD8+T细胞及各亚群频数及膜表面Tim-3表达水平的方法;q T-PCR检测血清中HCV-RNA水平;Spearman相关性分析CD8+T细胞频数、Tim-3表达与HCV-RNA之间的相关性。结果显示,慢丙肝患者外周血CD8+T细胞频数较健康对照组、IFN-α治疗组显著降低(P0.01)。初始T细胞明显增加(P0.01)。TCM、TEM细胞分布频率降低(P0.01)。经IFN-α治疗后,CD8+T细胞百分率上升(P0.05),初始T细胞数量下降(P0.01),TCM、TEM细胞频数均升高(P0.01)。三组人群TEMRA细胞频数无统计学差异。与健康对照组、IFN-α治疗组相比,慢丙肝患者CD8+T细胞及各亚群Tim-3表达水平均有上调(P0.05)。经抗病毒治疗后,CD8+T细胞、Naive细胞、TEM细胞、TEMRA细胞亚群Tim-3表达明显降低(P0.05),TCM细胞亚群中Tim-3表达也有降低,但无统计学差异。Spearman相关性分析发现:慢丙肝患者外周血CD8+T细胞百分率与病毒载量呈反比(r=-0.3775,P0.01),而Tim-3表达水平与病毒载量正相关(r=0.6230,P0.0001)。由此可知,HCV感染慢性化时可出现CD8+T细胞亚群分布异常及各亚群Tim-3过表达。IFN-α通过调节各CD8+T细胞亚群分化状态,及下调各群细胞表面Tim-3的表达,促进HCV免疫清除。     

肺癌患者放疗前后外周血淋巴细胞亚群变化研究

目的探讨肺癌患者放化疗前后外周血淋巴细胞亚群的变化.方法应用流式细胞仪对30例健康正常人群(对照组)和68例肺癌患者(肺癌组)放化疗前后的外周血T淋巴细胞亚群、B淋巴细胞及NK细胞等进行检测,并比较分析健康人群和肺癌患者的变化情况.结果肺癌组放疗前外周血中CD3~+,CD4~+,CD4~+/CD8~+,CD19~+与对照组相比均有所下降,差异均具有统计学意义(P0.05);CD8~+比例较对照组升高,且差异具有统计学意义(P0.05);而CD56~+比例较对照组升高,但结果无统计学意义(P0.05).肺癌患者放化疗后淋巴细胞亚群CD3~+降低,CD56~+有所升高,差异无统计学意义(P0.05);CD4~+,CD4~+/CD8~+较治疗前降低,CD8~+,CD19~+较治疗前升高,差异均具有统计学意义(P0.05).结论肺癌患者在疾病发生、发展过程中存在淋巴细胞免疫异常和免疫功能紊乱的现象,外周血T,B淋巴细胞及NK细胞的检测对判断患者的免疫功能有一定参考作用.     

慢性乙型肝炎患者外周血CD45RA+,CD45RO+T淋巴细胞亚群的特点及临床意义

目的 探讨慢性乙型肝炎患者外周血CD4＋CD45RA＋，CD4＋CD45RO＋，CD8＋CD45RA＋和CD8＋CD45RO＋T淋巴细胞亚群的特点及及其与肝病病情的关系．方法 采集46例轻中度慢性乙型肝炎患者、58例重度慢性乙型肝炎患者和30例健康人的外周抗凝血，应用流式细胞技术三色荧光分析法对其外周血中CD4＋CD45RA＋，CD4＋CD45RO＋，CD8＋CD45RA＋和CD8＋CD45RO＋T淋巴细胞亚群进行检测，结果轻中、重度慢性乙型肝楚患者与正常人相比．其外周血中CD4＋，CD8＋T细胞均无明显改变；CD8＋CD45RA＋T细胞均明显降低，CD8＋CD45RO＋T细胞均明显增高，而CD4＋CD45RA＋，CD4＋CD45RO＋T细胞均无明显改变；重度慢性乙型肝炎患者与轻中度慢性乙型肝炎患者相比，CD8＋CD45RA＋T细胞明显降低（P〈0．05），CD8＋CD45RO＋T细胞明显升高（P〈0．05）．结论乙型肝炎慢性化过程中，CD8＋CD45RO＋T细胞起重要作用且与慢性乙型肝炎患者病情的进展呈正相关；检测CD4＋CD45RA＋．CD4＋CD45RO＋．CD8＋CD45RA＋和CD8＋CD45RO＋T淋巴细胞亚群比检测CD4＋和CD8＋T细胞亚群能使我们更加正确、充分、全面地了解慢性乙型肝炎的发病机制和预后，从而有效地指导临床治疗。     

清疣饮对扁平疣患者体液免疫功能的影响

目的 探讨清疣饮对扁平疣患者血清中免疫球蛋白IgG ,IgA 和IgM含量的影响.方法 用琼脂扩散法定量测定血清免疫球蛋白.结果 患者血清IgG ,IgA 和IgM 水平升高.结论 清疣饮可以提高扁平疣患者体液免疫功能.     

胃癌及癌前病变患者外周血T淋巴细胞亚群的表达及意义

目的 探讨胃癌及癌前病变患者外周血T淋巴细胞亚群的表达情况.方法 收集20例慢性浅表性胃炎患者、20例胃癌前病变患者、38例胃癌患者血清标本,应用流式细胞仪检测外周血T淋巴细胞亚群表达水平,并进一步分析胃癌患者在不同分期、不同组织学分型及有或无淋巴结转移的T淋巴细胞亚群表达情况.结果 随着胃部疾病从浅表性胃炎-胃癌前病变-胃癌的逐渐进展,以及胃癌TNM分期的增加,胃癌发生淋巴结转移,外周血CD3+,CD4+T淋巴细胞表达逐渐降低,CD8+,CD25+T淋巴细胞表达逐渐升高.结论 外周血T淋巴细胞亚群的表达与胃癌发生、发展密切相关.     

丙肝患者PBMC mIL-2R及T细胞亚群检测

为了探讨丙型病毒性肝炎( 丙肝)患者膜白介素- 2 受体( mIL- 2R) 和 T 细胞亚群的表达水平及其在丙肝发病机理中的作用,用生物素- 链霉亲和素法对 203 例抗- HCV 阳性患者外周血单个核细胞进行 T 细胞亚群及植物血凝素( PHA) 诱导前后mIL- 2R 的检测. 总体结果显示丙肝患者外周血单个核细胞( PBMC) mIL- 2R 和 T 细胞亚群表达水平降低,与正常对照组相比,差异显著( P < 0. 01) .其中, 在静息状态和在 PHA 诱导状态,其 mIL- 2R 表达水平与正常对照组相比均低下( P < 0. 01) , 但急慢性丙肝患者中T 细胞亚群及 mIL- 2R 表达水平类似( P > 0. 05) . 急慢性丙肝患者与正常对照组相比,外周血 CD⁺₃ , CD⁺₄ 百分率降低, CD⁺₈ 百分率增高, CD⁺₄ / CD⁺₈ 比值下降( 从 P < 0. 05 降至 P< 0. 01) .说明丙肝患者体内存在明显的细胞免疫功能紊乱, T细胞活化障碍, 并与肝病的慢性化有关.     

MMP-2,MMP-9联合外周血T淋巴细胞亚群的变化对肺癌侵袭和转移预测研究

目的探讨血清基质金属蛋白酶(MMP-2,MMP-9)及T淋巴细胞亚群与肺癌临床类型及临床分期的关系.方法采用ELISA法测定各期肺癌患者血浆中MMP-2和MMP-9的含量,应用流式细胞仪进行外周血中T淋巴细胞的CD+3,CD+4,CD+8,CD+4/CD+8的测定.结果血清MMP-2,MMP-9外周血CD+8T淋巴细胞与NSCLC的分型无关,但高于对照组,CD+3,CD+4低于对照组;随着临床分期的增加,血清MMP-2,MMP-9明显增高,CD+3,CD+4,CD+8,CD+4/CD+8低于对照组,具有统计学意义.结论 MMP-2,MMP-9联合T淋巴细胞亚群可作为监测肺癌的发生、侵袭和转移更为精确的指标.     

半导体激光血管内照射对人体的免疫调节作用

报道了半导体激光血管内照射对人体外周血Ｔ淋巴细胞亚群及ＮＫ细胞的免疫调节作用，实验结果提示：在２３例患者中经波长６５０ｎｍ，功率５ｍＷ的半导体激光血管内照射治疗１次，５次和１０次的患者中，ＣＤ３＾＋细胞亚群的百分率与照射前（６３．６６％）比较，分别提高到６５．８６％，６９．９４％，７５．０４％；ＣＤ４＾＋Ｔ辅助细胞在第十次治疗后也有所增加，半导体激光血管内照射对ＮＫ细胞及ＣＤ４＾＋／ＣＤ８＾＋具有     

Expression of the gamma-delta T-cell receptor on intestinal CD8+ intraepithelial lymphocytes

The vast majority of mature T lymphocytes in the peripheral blood and lymphoid organs use the CD3-associated alpha, beta T-cell receptor (TCR) heterodimer for antigen recognition. A second class of TCRs consists of disulphide-linked gamma and delta proteins that are also CD3-associated. A subset of early CD3+ fetal and adult CD4- 8- thymocytes express gamma, delta TCRs before alpha, beta TCRs are detectable. In addition, a minor (1-5%) subpopulation of peripheral T lymphocytes, and some spleen cells from nude mice express gamma, delta TCRs. Notably, dendritic epidermal cells have also been shown to express gamma, delta TCRs. All of these populations lack CD4 and CD8 molecules. We now report that most mature T cells residing in the murine intestinal epithelium express CD3-associated TCRs composed of gamma-chains disulphide-linked to a protein resembling the delta-chain. The striking feature of these intraepithelial lymphocytes (IEL) was that they were exclusively CD4-8+. In addition, approximately half of CD3-bearing IEL lacked detectable Thy-1 on the cell surface, which is unprecedented for murine T cells. In contrast to other CD8+ peripheral T cells, freshly isolated IEL could be induced to display cytolytic activity by engaging the CD3 molecule, indicating that activation had occurred in vivo. Thus, CD8+ IEL are a phenotypically diverse and anatomically restricted population of lymphocytes that use gamma-chain containing heterodimers for antigen recognition.     

Differentiation potential of subsets of CD4-8- thymocytes

Precursor T cells in the thymus are contained within a subpopulation of thymocytes that lack the markers CD4 and CD8. We have examined the heterogeneity of these cells by flow cytometric analysis, and defined four subpopulations using the cell surface markers Thy-1, J11d and the IL-2 receptor (IL-2R). The J11d+ subset of CD4-8- cells all bear the antigen Thy-1, and some express the IL-2R. Staining and RNA analysis of J11d+ cells suggest that some express receptors of the CD3 gamma delta type, but none express CD3 alpha beta receptors. In fetal thymus organ culture, the J11d+ cells diversify to form 'cortical type' CD4+8+ cells and 'medullary type' cells expressing either CD4 or CD8; in vivo they repopulate the thymus of an irradiated host and seed the periphery with T cells. In contrast, the J11d- subset of CD4-8- thymocytes do not all bear Thy-1 and none express the IL-2R, but some express antigen receptors of the CD3 alpha beta type. They have more limited diversification potential in organ culture, and in vivo fail to recolonize the irradiated host in a homing-independent assay. We conclude that they are not precursor T cells, but rather a side-branch from the main line of T cell differentiation.     

脐带血T淋巴细胞集落培养和亚群的关系

应用细胞培养和间接免疫荧光法测定脐带血，成人外周血，成人骨髓的Ｔ淋巴细胞集落形成情况及培养前后淋巴细胞亚群的变化。结果表明：脐带血的ＣＦＵ－ＴＬ显低于成人外周血（Ｐ〈０．０１），略低地成人骨髓（Ｐ〈０．０５）；培养前脐带因的ＣＯ３、Ｃ含量均显低于成人外周血（Ｐ〈０．０１），成成人骨髓相近似。脐带血的ＣＤ８细胞含量与成人外周血和成人骨髓相似（Ｐ〈０．０５）；培养后的ＣＦＵ－ＴＬ中的ＣＴ３细胞含量     

细胞免疫在Tamm－Horsfal蛋白所致肾小管间质性肾炎组织损伤中的作用

采用Ｔａｍｍ－Ｈｏｒｓｆａｌ蛋白（ＴＨＰ）直接肾内注射建立大鼠的小管间质性肾炎（ＴＩＮ）模型，ＴＩＮ组９只动物均发生小管间质性组织病理损伤，局灶性单核、淋巴细胞炎症细胞浸润；对照组仅１只轻度炎症改变。外周血Ｔ淋巴细胞免疫表型分析，术后７ｄＴＩＮ组与对照组间ＣＤ＋４、ＣＤ＋８、ＣＤ＋８－ＣＤ＋２５、ＣＤ＋８－Ｉａ＋抗原的表达及ＣＤ４／ＣＤ８的比值均无显著性差异（Ｐ＞０．０５），而术后１４ｄ、ＴＩＮ组均见升高，与对照组比差异有显著性（Ｐ＜０．０５），表明ＴＩＮ组出现Ｔ淋巴细胞的免疫应答反应和活化性细胞毒Ｔ细胞明显增加，从而证实ＴＨＰ在致ＴＩＮ免疫发病机制中，确实存在免疫系统激活，导致肾间质炎症损伤     

Effect of lead exposure on the immune function of lymphocytes and erythrocytes in preschool children

Objective: To investigate the influence of lead exposure on the immune function of lymphocytes and erythrocytes in preschool children. Materials and methods: A group of 217 children three to six years of age from a rural area were given a thorough physical examination and the concentration of lead in blood samples taken from each subject was determined. The indices of lymphocyte immunity (CD^ 3CD^ 4, CD^ 3CD^ 8, CD^ 4CD^ 8, CDˉ3CD^ 19) and erythrocyte immunity (RBC-C3b, RBC-IC, RFER, RFIR, CD35 and its average fluorescence intensity) of 40 children with blood lead levels above 0.483 μmol/L were measured and compared with a control group. Results: The blood lead levels of the 217 children ranged from 0.11 μmol/L to 2.11 μmol/L. The CD^ 3CD^ 4and CD^ 4CD^ 8 cells were lower (P＜0.01) and the CD^ 3CD^ 8 cells were higher in the lead-poisoned subjects than those in the control group (P＜0.05). CD^ 3 and CDˉ3CD^ 19 did not show significant differences. Although the RBC-C3b rosette forming rate was lower and the RBC-IC rosette forming rate was higher in the lead-poisoned group, this difference could not be shown to be statistically significant (P＞0.05). RFIR was found to be lower in the lead-poisoned group (P＜0.01). Compared with the control group, the positive rate of CD35 was not found to be significantly different in a group of 25 lead-poisoned children (P＞0.05), while the average fluorescence intensity was lower in the lead-poisoned group (P＜0.05). Conclusion: Lead exposure can result in impaired immune function oft lymphocytes and erythrocytes in preschool children.     

Intrathymic deletion of self-reactive cells prevented by neonatal anti-CD4 antibody treatment

T-cell differentiation in the thymus involves the coordinate expression of genes encoding the alpha and beta chains of the major histocompatibility complex-restricted heterodimeric antigen receptor (TCR) complex, as well as other functionally important molecules such as CD4 and CD8. The repertoire of TCR expressed by T cells is generally thought to be influenced by positive and/or negative selection events occurring when TCRs on developing T cells interact with self-antigens and major histocompatibility complex components. Using a model system in which specific antigen-reactive cells can be monitored by virtue of their preferential expression of certain TCR beta-chain variable (V beta) domains, it has been shown that self-reactive T cells are clonally deleted during development. We report here that clonal deletion of V+ beta 6 cells in Mlsa mice can be prevented by in vivo neonatal administration of monoclonal antibodies directed against CD4. Furthermore, as anti-CD4 monoclonal antibody treatment resulted in the reappearance of V+ beta 6 cells in the mature CD8+ T-cell subset, it is likely that clonal deletion acts on the CD4+CD8+ thymocyte subset and that this subset is an intermediate stage in the differentiation pathway of both CD4+ and CD8+ T-cell lineages.     

Induction of cytotoxic T-cell responses in vivo in the absence of CD4 helper cells

Cytotoxic T lymphocytes (CTL) seem to provide the major line of defence against many viruses. CTL effector functions are mediated primarily by cells carrying the CD8 (Ly-2) antigen (CD8+ cells) and are triggered by interactions of the T-cell receptor with an antigenic complex, often termed 'self plus X', composed of viral determinants in association with class I molecules of the major histocompatibility complex (MHC). The mechanism(s) of induction of virus-specific CTL in vivo is poorly understood, but data from in vitro experiments suggest that their generation is strictly dependent on functions provided by CD4+ helper T cells (also referred to as L3T4+; or TH) that respond to antigens in the context of class II (Ia) MHC determinants. The prevailing opinion that induction of most functions of CD8+ cells requires help provided by CD4+ cells has recently been challenged by the observation that CD8+ cells alone can mediate a variety of responses to alloantigens in vitro and in vivo; however, the possibility that CTL to self plus X could be generated in vivo in the absence of TH cells has not been evaluated. We report here that C57BL/6J (B6) and AKR/J mice, when functionally depleted of CD4+ cells by in vivo treatment with the CD4+-specific rat monoclonal antibody GK1.5 (refs 8-14) responded to ectromelia virus infection by developing an optimal in vivo virus-specific CTL response, and subsequently recovered from the disease (mousepox) that was lethal for similarly infected nude mice (CD4-, CD8-).