血液CD3＋CD4＋／CD3＋CD8＋T细胞水平对肺部真菌感染的影响

目的探讨血液CD3＋CD4＋／CD3＋CD8＋T淋巴细胞水平对非HIV感染患者发生侵袭性肺部真菌感染的影响。方法根据入选标准及诊治规范,入选IPFI组患者61例,非IPFI肺炎组患者47例及同期健康对照组体检者30例。收集记录上述患者的临床资料,观察3组病例CD3CD;T淋巴细胞百分比,CD3＋CD8＋T淋巴细胞百分比及CD3＋CD4＋／CD3＋CD8＋T淋巴细胞比值情况。结果白色念珠菌仍是最常见的致病真菌,占总检出菌株数的46．03％,同时本研究曲霉菌（30．16％）感染也占有相当高的比例。CD3＋CD4＋T淋巴细胞百分比及CD3＋CD4＋／CD3＋CD8＋T细胞比值水平,IPFI组较非IPFI肺炎组（t=5．910,P〈0．05;t=7．395,P〈0．05）及健康对照组（t=6．443,P〈0．05;t=7．428,P〈0．05）均明显下降。结论血液CD4＋／CD8＋T淋巴细胞水平测定有助于早期发现肺部真菌感染的发生。     

Mice Chronically Infected with Chimeric HIV Resist Peripheral and Brain Superinfection: A Model of Protective Immunity to HIV

Infection by some viruses induces immunity to reinfection, providing a means to identify protective epitopes. To investigate resistance to reinfection in an animal model of HIV disease and its control, we employed infection of mice with chimeric HIV, EcoHIV. When immunocompetent mice were infected by intraperitoneal (IP) injection of EcoHIV, they resisted subsequent secondary infection by IP injection, consistent with a systemic antiviral immune response. To investigate the potential role of these responses in restricting neurotropic HIV infection, we established a protocol for efficient EcoHIV expression in the brain following intracranial (IC) inoculation of virus. When mice were inoculated by IP injection and secondarily by IC injection, they also controlled EcoHIV replication in the brain. To investigate their role in EcoHIV antiviral responses, CD8+ T lymphocytes were isolated from spleens of EcoHIV infected and uninfected mice and adoptively transferred to isogenic recipients. Recipients of EcoHIV primed CD8+ cells resisted subsequent EcoHIV infection compared to recipients of cells from uninfected donors. CD8+ spleen cells from EcoHIV-infected mice also mounted modest but significant interferon-γ responses to two HIV Gag peptide pools. These findings suggest EcoHIV-infected mice may serve as a useful system to investigate the induction of anti-HIV protective immunity for eventual translation to human beings.     

Simultaneous approach using systemic, mucosal and transcutaneous routes of immunization for development of protective HIV-1 vaccines

Mucosal tissues are major sites of HIV entry and initial infection. Induction of a local mucosal cytotoxic T lymphocyte response is considered an important goal in developing an effective HIV vaccine. In addition, activation and recruitment of memory CD4(+) and CD8(+) T cells in systemic lymphoid circulation to mucosal effector sites might provide the firewall needed to prevent virus spread. Therefore a vaccine that generates CD4(+) and CD8(+) responses in both mucosal and systemic tissues might be required for protection against HIV. However, optimal routes and number of vaccinations required for the generation of long lasting CD4(+) and CD8(+) CTL effector and memory responses are not well understood especially for mucosal T cells. A number of studies looking at protective immune responses against diverse mucosal pathogens have shown that mucosal vaccination is necessary to induce a compartmentalized immune response including maximum levels of mucosal high-avidity CD8(+) CTL, antigen specific mucosal antibodies titers (especially sIgA), as well as induction of innate anti-viral factors in mucosa tissue. Immune responses are detectable at mucosal sites after systemic delivery of vaccine, and prime boost regimens can amplify the magnitude of immune responses in mucosal sites and in systemic lymphoid tissues. We believe that the most optimal mucosal and systemic HIV/SIV specific protective immune responses and innate factors might best be achieved by simultaneous mucosal and systemic prime and boost vaccinations. Similar principals of vaccination may be applied for vaccine development against cancer and highly invasive pathogens that lead to chronic infection.     

Cytomegalovirus and the aging population

Human cytomegalovirus (HCMV) has the largest genome of any virus known to infect man. The virus has evolved many strategies to manipulate the host immune systems and so can remain latent and evade important immune responses. The human host mounts a substantial immune response against the virus, with up to 1% of the virus-specific CD8+ T cells being directed against specific epitopes. Acquisition of HCMV occurs progressively from an early age, and in developed countries the overall seroprevalence is approximately 60%. In contrast, specific communities such as gay men, lower socioeconomic groups and people residing in developing countries have seroprevalence rates that can exceed 90%. It is a widely held belief that successful control of viral infections decreases with increasing age because of a reduction in the capacity of the immune system. Studies in aging populations have shown a specific expansion of the CD8+, CD28- and CD57+ subset of cells in patients who are HCMV-seropositive. Prior infection with HCMV has also been associated with a significantly increased number of CD4+ and CD8+ lymphocytes, as well as cells expressing CD56 and HLA-DR. Thus, HCMV infection can cause substantial perturbations in T cell subsets and these effects persist in the aging population. In the context of solid organ transplantation, older age of both recipients and donors may serve to increase the frequency of donor-positive recipient-positive (D+R+) transplants, which have only a moderate risk of HCMV disease. In the context of HIV infection, age has been a dominant risk factor for progression to AIDS and death. At present, it does not appear that this can be explained by lack of immune control of HCMV in the aging population, although studies have identified prior HCMV infection as a risk factor for AIDS and death independent of age. We await further investigations to determine whether the immune control of HCMV in the elderly patient is as effective as in the younger adult, and whether this is linked to pathological consequences.     

HLA-E up-regulation induced by HIV infection may directly contribute to CD94-mediated impairment of NK cells

Alterations in NK cell numbers and function have been repeatedly shown during HIV infection. In this study, NK cell number and MHC class I expression on CD4+ T cells were studied in HIV patients at different stages of disease progression. An increased expression of HLA-E was seen on CD4+ T cells. In parallel, a reduced number of CD94+ NK cells was observed in advanced disease stages. Moreover, a decline in CD94 expression on NK cells was observed at the HIV replication peak in patients undergoing antiretroviral treatment interruption, suggesting a role of viral replication on NK cells alterations. In vitro HIV infection induced a rapid down-regulation of HLA-A,B,C expression, paralleled by an increased expression of HLA-E surface molecules, the formal ligands of CD94 NK receptors. HIV-infected HLA-E expressing cells were able to inhibit NK cell cytotoxicity through HLA-E expression, since cytotoxicity was restored by antibody masking experiments. These data indicate that the CD94/HLA-E interaction may contribute to NK cell dysfunction in HIV infection, suggesting a role of HIV replication in this process.     

CD59在艾滋病感染者CD4^＋T细胞表达及凋亡的影响

目的探讨补体调节蛋白CD59在艾滋病（HIV）感染者外周血CD4^＋T细胞上的表达及与凋亡之间的关系。方法收集12例确诊HIV感染者外周血标本（观察组）,同时收集10例健康对照者外周血标本（对照组）。分离外周血单个核细胞（PBMC）,并进行细胞表面染色。使用BDFACSCanto流式仪检测各项指标,采用FACSDiva软件分析CD4^＋T细胞CD59的表达情况,并分析CD59^＋CD4^＋T、CD59^-CD4^＋T细胞的凋亡情况。结果观察组CD4^＋T细胞CD59表达明显高于对照组（t=5．198,P〈0．01）;CD59＋CD4^＋细胞凋亡比率明显升高（t=5．968,P〈0．01）;而CD59^-CD4^＋T细胞的凋亡比例二组间差异无统计学意义（t=0．1353,P=0．8577）。结论HIV感染可引起CD4^＋T细胞补体调节蛋白CD59的表达,而CD59的表达会使CD4^＋T细胞凋亡增加。     

Cell cycle dysregulation during HIV infection: perspectives of a target based therapy

Human immunodeficiency virus (HIV) infection is characterized by a severe depletion of both CD4+ and CD8+ T cells, representing the result of virus-mediated killing of infected lymphocytes and the programmed cell death (apoptosis) of the uninfected bystander cells. Since only a small fraction of T lymphocytes are depleted by viral killing, apoptosis represents one of the most important mechanism of T cell death during HIV infection. Several apoptotic pathways can be triggered by the different stimuli: persistent T lymphocyte activation; altered death receptor (Fas, TNF-R, TRAIL R1-R2) membrane expression; viral proteins as well as gp120, Tat, and Nef; host factors such as the unbalance of cytokine synthesis by lymphocyte. Nevertheless, new evidences have demonstrated that the persistent HIV induced T cell activation and proliferation cause a cell cycle dysregulation resulting in a 5-fold increase in apoptotic cells. This perturbation represents a link between HIV infection, T cell activation, accelerated cell turnover and increased apoptosis and may thus represent a new therapeutic target. In fact, Interleukin-2 administration reverts such a cell cycle dysregulation and reduces activation induced T cell apoptosis. Herein we analyze the main HIV-related mechanisms of host cell death, that are dysregulation of the cell cycle and apoptosis induction of T lymphocytes. Finally, the role of cytokines at the site of infection and their association with apoptosis will be discussed to get insights into the immunological perturbations accounting for an accelerated disease progression. Current therapeutic approaches and strategies, like HAART and recombinant cytokines, that may, successfully, improve the immune-system dysregulation, are also discussed.     

类风湿关节炎合并肺部感染患者外周血T淋巴细胞和NK细胞水平及其临床意义

目的探究类风湿关节炎(RA)合并肺部感染患者外周血T淋巴细胞和自然杀伤细胞(NK细胞)的水平及其临床意义。方法选取48例RA合并肺部感染患者作为RA合并感染组,64例RA未合并肺部感染患者作为RA未合并感染组,另选取同期于本院健康体检中心进行体检的30例健康成年人作为对照组。比较三组外周血T淋巴细胞亚群及NK细胞水平,比较稳定期与活动期RA合并与未合并肺部感染患者的T淋巴细胞亚群及NK细胞水平。结果RA合并感染组CD3⁺(641.21±438.08)个/μl、CD4⁺(171.58±96.42)个/μl、CD8⁺(215.48±110.16)个/μl、CD4⁺/CD8⁺(0.82±0.26)、NK细胞(26.57±4.88)个/μl;RA未合并感染组CD3⁺(1051.36±434.65)个/μl、CD4⁺(308.07±101.69)个/μl、CD8⁺(324.17±108.16)个/μl、CD4⁺/CD8⁺(0.96±0.24)、NK细胞(40.52±8.92)个/μl;对照组CD3⁺(1403.00±402.77)个/μl、CD4⁺(610.07±82.58)个/μl、CD8⁺(532.47±168.45)个/μl、CD4⁺/CD8⁺(1.35±0.21)、NK细胞(365.15±117.61)个/μl。RA合并感染组、RA未合并感染组CD3⁺、CD4⁺、CD8⁺、CD4⁺/CD8⁺、NK细胞水平均低于对照组,差异有统计学意义(P<0.05)。RA合并感染组CD3⁺、CD4⁺、CD8⁺、CD4⁺/CD8⁺、NK细胞水平均低于RA未合并感染组,差异有统计学意义(P<0.05)。稳定期RA合并肺部感染患者CD3⁺、CD4⁺、CD8⁺、CD4⁺/CD8⁺、NK细胞水平均低于稳定期RA未合并肺部感染患者,差异有统计学意义(P<0.05);活动期RA合并肺部感染患者CD3⁺、CD4⁺、CD8⁺、CD4⁺/CD8⁺、NK细胞水平均低于活动期RA未合并肺部感染患者,差异有统计学意义(P<0.05)。结论合并肺部感染的RA患者T淋巴细胞、NK细胞明显偏低,T淋巴细胞及NK细胞可能在一定程度上对RA合并肺部感染发挥一定的预测价值,指导临床诊疗。     

Prostaglandin E2 induces the expression of functional inhibitory CD94/NKG2A receptors in human CD8+ T lymphocytes by a cAMP-dependent protein kinase A type I pathway

The CD94/NKG2A heterodimer is a natural killer receptor (NKR), which inhibits cell-mediated cytotoxicity upon interaction with MHC class I gene products. It is expressed by NK cells and by a small fraction of activated T cells, predominantly of CD8+ phenotype. Abnormal upregulation of the CD94/NKG2A inhibitory NKR on cytotoxic T cells (CTLs) could be responsible for a failure of immunosurveillance in cancer or HIV infection. In an attempt to identify the mechanisms leading to inhibitory NKR upregulation on T cells, we analyzed the expression of the CD94/NKG2A heterodimer on human CTLs activated with anti-CD3 mAb in the presence of PGE2 or with 8-CPT-cAMP, an analogue of cyclic AMP. As previously described, anti-CD3 mAb-mediated activation induced the expression of CD94/NKG2A on a small fraction of CD8+ T cells. Interestingly, when low concentrations of PGE2 or 8-CPT-cAMP were present during the culture, the proportion of CD8+ T cells expressing CD94/NKG2A was two- to five-fold higher. This upregulation was partially prevented by PKA inhibitors, such as KT5720 and Rp-8-Br-cAMP (type I selective). We also report that cAMP induces upregulation of NKG2A at the mRNA level. We further demonstrated that cross-linking of CD94 on CD8+ T cells expressing the CD94/NKG2A heterodimer inhibits their cytotoxic activity in a bispecific antibody redirected lysis assay. Our findings clearly demonstrate that the PGE2/cAMP/PKA type I axis is involved in the expression of CD94/NKG2A receptor on human CD8+ T lymphocytes.     

慢性乙型肝炎病毒感染者外周血T细胞亚群变化与其血清HBV DNA的水平分析

目的:观察慢性乙型肝炎病毒(HBV)感染者细胞免疫功能的变化,探讨病毒复制程度与细胞免疫功能的关系。方法:应用流式细胞仪直接免疫荧光法检测136例乙肝病毒感染者、60例正常对照者外周血T淋巴细胞亚群百分率,用荧光定量聚合酶链式反应(PCR)法检测乙型肝炎感染者血清HBV DNA。结果:84例慢性HBV携带者(ASC)、52例慢性乙型肝炎(CHB)患者与健康对照组相比,CD3+ T淋巴细胞百分比、CD4+T淋巴细胞百分比和CD4+/CD8+ T淋巴细胞比值均显著降低(P<0.001),CD8+ T淋巴细胞百分比均显著升高(P<0.001)。慢性乙型肝炎患者与慢性HBV携带者相比,CD3+ T淋巴细胞百分比差异无统计学意义(P>0.05)、CD4+ T淋巴细胞百分比明显降低(P<0.05)、CD8+ T淋巴细胞百分比明显升高(P=0.01)、CD4+/CD8+ T淋巴细胞比值明显降低(P<0.05)。随着病情发展,从健康对照组、慢性HBV携带者到慢性乙型肝炎,CD4+T淋巴细胞百分比、CD4+/CD8+比值呈逐渐下降趋势,CD8+ T细胞百分比呈逐渐升高的趋势。慢性HBV携带者HBV DNA阳性组与HBV DNA阴性组相比,CD3+ T淋巴细胞差异均无统计学意义(P>0.05),CD4+ T淋巴细胞百分比明显下降(P<0.001),CD4+/CD8+ T淋巴细胞比值明显下降(P<0.001),CD8+ T淋巴细胞百分比明显升高(P<0.01)。结论:HBV感染可导致感染者细胞免疫功能的改变,HBA DNA复制增加进一步加重乙肝病毒感染者T细胞亚群的紊乱,CD4+/CD8+ T淋巴细胞比值的动态变化可及时提示临床HBV感染者细胞免疫功能的变化并加强临床的监测。     

慢性乙型肝炎病毒感染对外周血单个核细胞中凋亡分子表达的影响及其与免疫功能的相关性

目的 研究慢性乙型肝炎病毒(HBV)感染对外周血单个核细胞中凋亡分子表达的影响及其与免疫功能的相关性.方法 选择76例慢性乙型肝炎(CHB)患者和体检的54例健康志愿者,分别作为CHB组和对照组,采集血清并测定凋亡分子含量、采集外周血单个核细胞并测定凋亡分子表达量以及免疫细胞含量.结果 CHB组患者血清中凋亡分子Fas、FasL、Caspase-3、Caspase-6、Caspase-8的含量以及外周血单个核细胞中Fas、FasL、Caspase-3、Caspase-6、Caspase-8的mRNA含量均显著高于对照组;CHB组患者外周血中CD3+ CD4+T细胞、CD3+ CD8+T细胞、CD16+ CD56+ NK细胞的百分比及CD4+/CD8+的比例均显著低于对照组;外周血单个核细胞中Fas、FasL、Caspase-3、Caspase-6、Caspase-8的mRNA含量与CD3+ CD4+T细胞、CD3 +CD8+T细胞、CD16+ CD56+自然杀伤(NK)细胞的百分比呈负相关.结论 慢性HBV感染能够增加外周血单个核细胞中凋亡分子的表达,进而造成T淋巴细胞和NK细胞凋亡、抑制细胞免疫应答和非特异性免疫应.     

Lymphocyte expression of EZH2 is associated with mortality and secondary infectious complications in sepsis

Recent studies have shown that epigenetic factors may affect immune responses. We previously reported that histone methyltransferase enhancer of zeste homolog 2 (EZH2) was involved in the innate inflammatory responses both in animal model of sepsis and in septic patients. In this study, we prospectively evaluated EZH2 expression kinetics in peripheral CD4+ and CD8+ T cells and HLA-DR expression in CD14+ cells from 48 patients with sepsis and 48 healthy controls. Results showed higher level of EZH2 in CD4+ T cells and CD8+ T cells in sepsis patients than in controls. Meanwhile, EZH2 expression was correlated with CD27 status on T cells. Mean fluorescence intensity (MFI) of EZH2 in CD8+ T cells on day 1 independently predicted death in septic patients. Also, the combination of CD8+ T cell EZH2 expression with APACHEII and SOFA score could enhance the prognostic predictive ability. Moreover, multivariate logistic regression analysis showed that increased expression (proportion and MFI) of EZH2 in CD4+ and CD8+ lymphocytes on day 3 were independently associated with nosocomial infection in septic patients. Additionally, spearman correlation analysis indicated that the levels of EZH2 in CD4+ T cells and CD8+ T cells correlated to CD14+ cells-expressing HLA-DR in patients with sepsis at each time point. Overall, these findings suggest that EZH2 in CD4+ T cells or/and CD8+ T cells may be a novel biomarker for predicting adverse outcomes (mortality and secondary infectious complications) in patients with sepsis.     

Higher levels of HIV DNA in memory and naive CD4(+) T cell subsets of viremic compared to non-viremic patients after 18 and 24 months of HAART

The degree of infection of memory and naive CD4⁺ T cells in patients treated with HAART and with durable undetectable or detectable viral load in plasma was evaluated. The following two groups of patients were analyzed cross-sectionally: (i) patients with undetectable HIV RNA plasma levels during follow-up (responders); (ii) patients with no reduction or with rebound in HIV RNA levels during treatment (non-responders). Patients were examined following 6, 12, 18 and 24 months of HAART, respectively, by quantifying: (i) plasma HIV RNA load; (ii) CD4⁺ T cells; (iii) memory and naive CD4⁺ T cells; (iv) HIV DNA levels in memory and naive CD4⁺ T cells. HIV RNA plasma levels were significantly higher in non-responders vs responders at each time point (P<0.02), while CD4⁺ T cell counts as well as memory and naive CD4⁺ T cell levels were comparable in both viremic and non-viremic patients. However, higher HIV DNA values were observed in both memory and naive CD4⁺ T cells of non-responders vs responders after 18 and 24 months of HAART (P<0.02), suggesting an increased amount of HIV-infected naive CD4⁺ T cells and a sustained high degree of infection of memory CD4⁺ T cells. Immunological reconstitution following HAART might potentially be hampered in viremic patients despite the absolute increase in CD4⁺ T cell counts.     

肺肿瘤小鼠MDSC、 Treg 及传统T 细胞变化研究

摘要： 目的 探讨肺肿瘤小鼠骨髓源性抑制细胞 （MDSC）、 调节性 T 细胞 （Treg） 和传统 T 细胞的变化及机制。方法 采用配对设计将 20 只 C57BL/6 小鼠随机均分为 Lewis 肺癌细胞注射组 （LLC 组） 和正常对照组 （NC 组）, LLC 组采用皮下注射 LLC 细胞 100 μL （1×106 ） 制备肺肿瘤小鼠模型, 对照组注射等量生理盐水。待肿瘤形成后取小鼠脾细胞, 采用流式细胞仪检测肺肿瘤小鼠 MDSC、 Treg 及 CD4+ 和 CD8+ T 细胞比例和数量变化, 膜联蛋白-V （Annexin-Ⅴ）染色检测 CD4+ 和 CD8+ T 细胞凋亡变化, 5-溴脱氧尿嘧啶核苷 （BrdU） 染色检测 CD4+ 和 CD8+ T 细胞增殖变化。结果 与 NC 组相比, LLC 组脾脏 MDSC 比例和数量明显增加, CD4+ Foxp3+ Treg 所占 CD4+ T 细胞比例和数量明显增加,而 CD4+ 和 CD8+ T 细胞所占脾细胞比例和数量明显降低 （均 P < 0.05）。与 NC 组相比, LLC 组 CD4+ 和 CD8+ T 细胞增殖明显降低, 同时 CD8+ T 细胞凋亡明显增加 （P < 0.05）。结论 MDSC 和 Treg 细胞在肺肿瘤小鼠数量增加, 同时, MDSC 和Treg 抑制 CD4+ 和CD8+ T 细胞增殖, 并促进 CD8+ T 细胞凋亡。     

Do Opioids Activate Latent HIV-1 by Down-Regulating Anti-HIV microRNAs?

Researchers have recently demonstrated the presence of anti-HIV-1 microRNAs (miR-28, miR-125b, miR-150, miR-223, and miR-382) in monocytes, macrophages, and CD4+ T cells, which are the primary targets of HIV infection. These miRNAs appear to regulate the level of infectivity of HIV-1 in the target cells, and thus have an impact on HIV-1 latency. The levels of these miRNAs are significantly higher in resting CD4+ T cells than those in active CD4+ T cells, whereas HIV-1 infectivity is greater in active than in resting CD4+ T cells. Similarly, the levels of these miRNAs are significantly higher in monocytes than in macrophages, whereas HIV-1 infectivity is greater in macrophages than in monocytes. Down-regulation or inhibition of the activity of these miRNAs can promote replication of latent HIV-1 in resting CD4+ T cells and in monocytes. Recently, morphine was shown to down regulate the expression of anti-HIV miRNAs (miRNA-28, 125b, 150, and 382) in cultured human monocytes and this effect of morphine was mediated via activation of mu opioid receptors (MOR). In addition, levels of these anti-HIV miRNAs were significantly lower in the peripheral blood mononuclear cells (PBMCs) isolated from heroin-dependent subjects than those from control subjects. These findings raise an important question: Does morphine have potential to activate latent HIV-1 in resting CD4+ T cells and macrophages, including microglia of human subjects maintained on highly active antiretroviral therapy (HAART)? Further research is required to answer this question.     

急性和慢性EB病毒感染儿童外周血CD8+T 细胞活化差异

摘要 目的：比较急性和慢性EB病毒感染儿童总T细胞,CD8+T细胞及CD8+T 细胞活化HLA-DR表达的差异,探讨不同感染形式的不同发病机制。方法：应用流式细胞术检测27例急性EB病毒感染儿童,7例慢性EB病毒感染儿童和29例对照组儿童外周血淋巴细胞中总T细胞,CD8+T细胞和CD8+T细胞活化HLA-DR表达水平,并对急性和慢性感染儿童各项检测指标之间进行比较。 结果：急性EB病毒感染儿童总T细胞,CD8+T细胞, CD8+/HLA-DR+细胞明显高于慢性EB病毒感染儿童和对照组（p<0.01）;慢性EB病毒感染儿童总T细胞低于对照组,CD8+/HLA-DR+细胞高于对照组（p<0.01）。结论：急性和慢性EB病毒感染儿童总T细胞,CD8+T细胞及CD8+T 细胞活化HLA-DR表达存在明显差异,慢性EB病毒感染儿童CD8+T 细胞处于低水平活化状态,CD8+T细胞活化水平检测可作为评估EB病毒感染患儿细胞免疫功能的有效指标。     

EB病毒感染患儿的免疫功能研究

目的：了解EB病毒（EBV）感染疾病类型与患儿免疫功能的关系。方法：选取2010年12月至2015年12月我院儿科收治的EBV感染儿童80例（EBV感染组）以及同期在我院体检的正常儿童38例（对照组）,采用散射比浊法检测血清免疫球蛋白和补体,采用流式细胞仪检测外周血淋巴细胞分化抗原T淋巴细胞（CD3+）、辅助性T细胞（CD4+）、细胞毒性T细胞（CD8+）、B淋巴细胞（CD19+）及NK细胞（CD56+）阳性率以及CD4+/CD8+。结果：两组IgA水平比较差异无统计学意义（P>0.05）。EBV感染组IgM、IgG、IgE、C3和C4表达均升高,与对照组比较差异均有统计学意义（P<0.05）。EBV感染组CD3+、CD8+、CD19+、CD56+计数高于对照组,CD4+、CD4+/CD8+低于对照组,差异有统计学意义（P<0.05）。结论：EBV感染疾病与患儿的免疫功能相关,与CD4+ T细胞和B细胞计数减少有明显的关系,可以采用外周血淋巴细胞分化抗原测定方法检测EBV感染后的淋巴细胞亚群变化。     

How does indoleamine 2,3-dioxygenase contribute to HIV-mediated immune dysregulation

Infection with the human immunodeficiency virus type 1 (HIV) results in a chronic infection that progressively cripples the host immune defenses. HIV infection is associated with increased tryptophan (trp) catabolism by the cytokine-inducible enzyme indoleamine 2,3-dioxygenase (IDO). IDO has powerful immune suppressive activity, which could contribute to the immune dysfunction observed in HIV-infected patients. In this review we discuss the immune mechanisms that could mediate the HIV-induced increase of IDO activity (such as IFN-gamma, IFN-alpha, CTLA-4/B7 and direct viral exposure). We then consider the current knowledge of IDO-mediated immune suppressive mechanisms with regard to different cell types (CD4(+) T cells, CD8(+) T cells, natural killer cells, B cells and regulatory T cells), from the perspective of their potential consequences for the HIV-infected host. HIV-induced, IDO-mediated trp catabolism may contribute to the perpetuation of HIV infection into its chronic phase by dampening efficient immune anti-viral responses. Therapeutic approaches aimed at manipulating this powerful immune suppressive mechanism might be considered in the setting of HIV infection.