类风湿关节炎患者外周血单核细胞亚群的变化及其意义

目的:本次研究通过检测类风湿关节炎(RA)患者外周血单核细胞亚群比例及其分泌促炎细胞因子的功能,探讨单核细胞亚群在RA 发病过程中的作用。方法:22 例RA 患者(RA 组)和22 例健康对照者(HC 组),经知情同意后抽取3ml 静脉血,肝素钠抗凝。流式细胞术(FCM)检测单核细胞亚群比例、中间型单核细胞表面HLA-DR、Toll 样受体2(TLR2)和髓系细胞触发受体-1(TREM-1)表达,及其细胞内肿瘤坏死因子(TNF)鄄琢平均荧光强度(MFI),并分析RA 患者单核细胞亚群比例与血清细胞因子的相关性。正态数据分析采用Students’t-test 检验。结果:与HC 组相比,RA 组中间型单核细胞比例升高[(4.6±1.2)% vs (11.7±1.6)%],差异有统计学意义(P<0.05);HLA-DR 表达(MFI)与HC 组比较差异无统计学意义(26.8±8.6 vs 30.2±6.1,P>0.05)。RA 组TLR2(750.2±110.3 vs 526.8±98.6)、TREM-1(58.4±12.1 vs 40.3依10.2)表达(MFI)高于HC 组,差异均有统计学意义(P<0.05);RA 组中间型单核细胞胞内TNF鄄琢(46.3±6.4 vs 36.7±8.3)MFI 高于HC 组,差异有统计学意义(P<0.05)。RA 患者中间型单核细胞比例与DAS28 评分和血清TNF 、白细胞介素(IL)-17 呈正相关,相关系数分别为0.593(P =0.003)、0.471(P =0.027) 和0.538(P =0.009)。结论:RA 患者外周血单核细胞向中间型极化,并处于活化状态,高表达TLR2 和TREM-1,分泌较多的促炎细胞因子TNF ,参与RA 的疾病过程。因此,抑制单核细胞向中间型极化或阻断表面受体表达可能是治疗RA 的新途径。     

外周血淋巴细胞亚群在儿童EB病毒感染中的变化及临床意义

目的：探讨外周血淋巴细胞亚群在儿童EB病毒(EBV)感染诊断中的临床意义。方法：选取EBV感染患儿48例作为观察组，另选取急性支气管肺炎患儿23例和肺炎支原体(MP)感染患儿48例作为对照组。流式细胞术检测患儿外周血淋巴细胞亚群，并收集患儿临床资料。比较观察组与对照组、观察组传染性单核细胞增多症(IM)与非IM、肝功能异常与肝功能正常患儿淋巴细胞亚群变化。线性相关分析法分析观察组淋巴细胞亚群与血清EBV-DNA载量的相关性。受试者工作特征(ROC)曲线评估淋巴细胞亚群的诊断效能。结果：EBV感染患儿外周血淋巴细胞数量、T细胞数量和比例、CD8⁺T细胞数量和比例升高(均P<0.05),CD4⁺T细胞比例、B细胞比例及CD4⁺/CD8⁺降低(均P<0.05)。EBV感染患儿外周血淋巴细胞改变与EBV-DNA载量相关。与非IM和肝功能正常患儿相比，IM和肝功能异常患儿淋巴细胞数量(均P<0.001)、T细胞数量(均P<0.001)和比例(P<0.001;P=0.002)、CD...     

炎性关节炎患者调节性T细胞亚群的变化及其对TNF-α拮抗剂治疗的反应

人外周血CD4+Foxp3+调节性T细胞(regulatory T cells,Treg)的表型和功能存在异质性。本文用Foxp3和CD45RO共同标记Treg,研究强直性脊柱炎(AS)和类风湿性关节炎(RA)患者外周血Treg亚群数量以及接受TNF-α拮抗剂治疗对其亚群的改变。分别采集未经治疗的21例活动性AS患者和27例活动性RA患者的外周血。两种疾病各有14名患者接受TNF-α拮抗剂治疗40周。应用流式细胞术检测外周血Treg细胞数量。在CD4+T细胞中,活动性AS和RA患者其表型为CD45RO+Foxp3hi的效应型Treg(AS与正常对照相比,P=0.020;RA与正常对照相比,P0.001)和表型为CD45RO-Foxp3low的幼稚型Treg(AS与正常对照相比,P=0.009;RA与正常对照相比,P=0.001)细胞数量均显著下降。与正常对照相比,AS和RA患者的CD4+Foxp3+T细胞中非Treg亚群细胞(表型为CD45RO+Foxp3low)的比例显著增加(AS与正常对照相比,P=0.027;RA与正常对照相比,P0.001)。TNF-α拮抗剂治疗后,AS患者外周血中效应型Treg(P=0.025)和幼稚型Treg(P=0.005)细胞数量均增加,RA患者中仅效应型Treg细胞数量增加(P=0.003)。因此,不仅分析CD4+Foxp3+T细胞总数,而且分析其中不同表型的亚群细胞数量更有助于明确炎性关节炎的发病机制。     

重症肌无力患者外周血CD28~-T细胞亚群变化及临床意义

检测重症肌无力(MG)患者外周血CD28-T细胞亚群的变化,并探讨其临床意义。收集46例MG患者和35例健康对照(HC)外周血标本,采用免疫荧光染色和流式细胞术检测外周血CD4+CD28-和CD8+CD28-T细胞亚群。结果显示,MG患者和HC比较,前者CD28表达下调,CD4、CD8表达无差异;MG患者CD4+CD28-T细胞亚群(13.53%±6.31%)较HC(9.24%±4.62%)异常升高(P=0.001),而CD8+CD28-T细胞亚群(39.22%±11.91%)较HC(48.41%±13.63%)显著下降(P=0.002);全身型MG(GMG)和并发胸腺异常的MG患者中,CD4+CD28-T细胞亚群比例分别较眼肌型MG(OMG)和正常胸腺MG患者升高,而CD8+CD28-T细胞亚群百分比明显下降;QMGS评分与CD4+CD28-T细胞亚群呈正相关(r=0.4113,P=0.0045),而与CD8+CD28-T细胞亚群呈负相关(r=-0.3989,P=0.0060);激素治疗后伴随CD4+CD28-T细胞比例下降(P=0.018)和CD8+CD28-T细胞比例升高(P=0.018)。本研究发现,MG患者外周血CD4+CD28-T细胞亚群比例升高和CD8+CD28-T细胞亚群比例下降与疾病严重程度、治疗反应密切相关,且在不同临床分型的MG患者中存在差异性变化。上述提示CD28-T细胞亚群的异常变化可能参与了MG的免疫病理进程。     

Tim-3和PD-1在慢性丙型肝炎患者不同单核细胞亚群的表达水平分析

目的分析慢性丙型肝炎(CHC)患者外周血单核细胞亚群分布,同时观察负性调节分子T细胞免疫球蛋白及黏蛋白域蛋白3(Tim-3)和程序性细胞死亡蛋白1(PD-1)在各亚群表达的变化及意义。方法利用流式细胞术检测CHC患者外周血单核细胞亚群比例和各亚群Tim-3、PD-1表达,并与临床指标如丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)采用Spearman方法进行相关性分析。结果与健康对照组比较,CHC患者外周血CD14~+CD16~+单核细胞比例增高,以CD14CD16~+单核细胞比例增高显著。Tim-3在CD14CD16-单核细胞和CD14~+CD16单核细胞上表达水平升高;PD-1在CD14CD16-单核细胞和CD14CD16~+单核细胞上表达水平升高。CHC患者单核细胞亚群以及各亚群Tim-3、PD-1和临床指标ALT及AST无明显相关性。结论 Tim-3和PD-1在不同单核细胞亚群表达水平不同。     

中性粒细胞CD64的表达对重症手足口病患儿的诊断价值

目的:探讨中性粒细胞CD64的表达对重症手足口病患儿的诊断价值。方法:选择在我院住院的手足口病初诊患儿共134例,其中重症组为52例,普通组为82例,应用流式细胞术测定中性粒细胞CD64,同时测外周血C反应蛋白(CRP)、白细胞及分类。结果:重症组CD64水平为(14.11±9.08)平均荧光强度(MFI),明显高于一般感染组(10.75±3.88)MFI(P<0.05),以CD64≥10.5MFI为阳性标准,CD64在重症组的阳性率为51.9%,普通组患儿为10.9%,两者阳性率有统计学差异(P<0.01)。结论:中性粒细胞CD64的表达适用于重症手足口病感染病情的监测,而且还可作为抗生素应用的依据。     

RA患者外周血CD141~+DCs数量的变化及其与Tregs的关系

目的探讨RA患者外周血各DCs亚群数量的变化,为进一步阐明RA的发病机制奠定基础。方法选取63例RA患者和30例相匹配的健康体检者作为正常对照组,将入选的RA患者根据疾病活动性评分(DAS28)分为3个亚组。采用流式细胞术检测所有受试者外周血DCs、Treg细胞比例并分析各DC亚群与Treg的相关性。结果 RA患者外周血总的DCs数量低于正常对照组(P0.05);RA患者pDCs的比例与正常对照组无差异(P0.05);CD1C~+DCs比例降低,但无统计学意义(P0.05);CD141~+DCs比例明显下降(P0.01),并与Tregs的变化一致,r=0.51,P0.01。结论 RA患者的CD141~+DCs比例下降与Tregs的下降有关,可能在RA的发病中起到一定的作用。     

慢性乙型肝炎患者外周血单核细胞Tim-3表达的检测及意义

目的 研究慢性乙型肝炎(CHB)患者外周血单核细胞中T淋巴细胞免疫球蛋白黏蛋白分子3(Tim-3)的表达及对其炎症因子生成的影响.方法 利用多色流式技术和荧光实时定量PCR(qRT-PCR),分别检测不同状态的CHB患者外周血单核细胞亚群表面Tim-3分子和Tim-3 mRNA表达水平.给予重组人galectin-9和脂多糖(LPS)共刺激CHB活动期患者外周血单核细胞,用ELISA检测培养上清中TNF-α、IL-1β和IL-6水平.结果 慢乙肝免疫耐受期患者(IT)外周血单核细胞表面Tim-3表达水平显著高于健康对照组(HC)和免疫活动期患者(IA)(P＜0.01),其中IT患者CD14+ CD16-和CD14+ CD16+单核细胞亚群中Tim-3的表达均高于IA患者,差异均有统计学意义.qRT-PCR结果进一步证实IA患者外周血单核细胞中Tim-3 mRNA的表达高于HC (P =0.040).IA患者CD14+单核细胞上Tim-3的表达与血清丙氨酸氨基转移酶(ALT)水平呈正相关(r=0.362,P=0.028).重组人galectin-9和LPS共刺激IA患者外周血单核细胞比单独使用LPS刺激分泌更高水平的TNF-α,IL-1,IL-6.结论 CHB患者外周血单核细胞Tim-3表达上调,与血清ALT水平呈正相关,Tim-3/galeetin-9通路能够促进LPS诱导的单核细胞的炎症因子的分泌.     

HIV/AIDS患者外周血CD4~+T细胞亚群及中性粒细胞CD64的变化及临床意义

目的探讨HIV/AIDS患者外周血中CD4+T细胞亚群及中性粒细胞CD64的变化及临床意义。方法筛选2014年5月至9月河南中医学院第一附属医院艾滋病临床研究中心收治的47例HIV/AIDS患者,根据CD4+T淋巴细胞数将其分为A组(CD4≤350 cell/μl)23人,B组(CD4350 cell/μl)24人,同期选取健康对照组20人。用流式细胞仪(FCM)检测3组人员外周血中CD4+T细胞亚群(Th1、Th2、Th17、Treg)及中性粒细胞表面CD64表达水平,用SPSS17.0软件分析数据。所有数据用中位数表示,2组间比较采用Mann-Whitney检验,相关性分析采用Spearman秩相关。结果 A组和健康对照组Th1细胞(CD4+IFN-γ+)百分比均高于B组(P=0.040,P=0.028);A组Th2细胞(CD4+IL4+)百分比高于B组(P=0.015);A和B组Treg细胞(CD4+CD25+FOXP3+)百分比均高于健康对照组(P均0.05),A组Treg细胞高于B组(P=0.001);Th17细胞以及中性粒细胞表面CD64的表达量3组比较差异无统计学意义;Treg细胞与CD4+T细胞呈负相关(r=-0.734,P=0.000),Treg细胞与Th1/Th2比值呈负相关(r=-0.300,P=0.015)。结论 HIV/AIDS患者CD4+T细胞亚群之间的平衡失调,调节性T细胞处于优势状态,CD4+T细胞亚群变化可作为HIV/AIDS患者疾病进展的动态监测指标。CD64是机体急性炎症感染的一个重要参考指标,但在HIV/AIDS患者中变化不明显。     

CD38在类风湿关节炎外周血与滑膜组织中的表达

CD38是单链Ⅱ型跨膜蛋白,为B淋巴细胞活化的标记物。类风湿关节炎(rheumatoid arthritis,RA)是自身免疫性疾病,病变滑膜内存在大量B淋巴细胞增生。本研究通过对RA患者外周血及滑膜中的CD38进行表达分析从而探寻RA发病的免疫机制。应用流式细胞术检测RA患者(N=103)及正常人(N=120)外周血中CD38的表达;采用免疫组织化学法分别对5例RA患者、骨关节炎(osteoarthritis,OA)患者及强直性脊柱炎(ankylosing spondylitis,AS)患者滑膜组织中CD38的表达进行检测;将靶向CD38的SiRNA转入RA患者滑膜成纤维细胞(RASF)(N=5)后,ELISA法检测培养基中TNF-α、IL-1α和IL-β的表达。流式结果显示RA患者外周血中CD38+(P=1.92E-09)、CD3+CD38+(P=0.019)和CD56+CD38+(P=0.007)亚群细胞表达率明显升高,且CD38+细胞的表达率与RA患者类风湿因子(RF)水平显著相关(P=0.026);免疫组织化学结果表明CD38在RA患者滑膜中特异性高表达;ELISA实验证实:对CD38基因进行SiRNA干扰后,RASF培养基中的IL-1α和IL-1β表达水平显著降低。该项研究表明:CD38基因的表达增加可能参与RA患者的免疫激活。     

Monocyte subsets study in children with Mycoplasma pneumoniae pneumonia

The aim of this study was to evaluate the changes in the three subsets of monocyte (classical, intermediate, and non-classical) and the expression of human leukocyte antigen-DR (HLA-DR) on monocyte subsets during MP pneumonia in children. Monocyte subsets were analyzed in the peripheral blood of healthy volunteers and MP pneumonia patients at the stages of admission and remission after clinical therapy. They were defined as classical (CD14⁺CD16⁻), intermediate (CD14^brightCD16⁺), and non-classical (CD14^dimCD16⁺) using flow cytometry. Furthermore, three subsets of monocyte were analyzed for the expression of HLA-DR. Patients with MP pneumonia at admission had a higher proportion of intermediate and non-classical monocytes than healthy subjects (all P < 0.05). The proportion of intermediate subset and non-classical subset was lower in MP pneumonia patients at remission than at admission (all P < 0.05). In comparison with the other monocyte subsets, intermediate subset showed a significantly higher percentage of HLA-DR in MP pneumonia patients at admission (P < 0.05). Further analysis revealed that the expression of HLA-DR on intermediate subset was lower in severe patients than in non-severe patients (P < 0.05).Our data has shown for the first time that MP pneumonia is associated with the increased proportion of non-classical and intermediate monocytes, indicating the involvement of monocyte-related mechanisms in the pathogenesis of this disease. Additionally, the decreased expression of HLA-DR on CD14^brightCD16⁺ subset may be a potential indicator of the severity of MP pneumonia.

     

CD14 expression is increased on monocytes in patients with anti‐neutrophil cytoplasm antibody (ANCA)‐associated vasculitis and correlates with the expression of ANCA autoantigens

Monocyte subsets with differing functional properties have been defined by their expression of CD14 and CD16. We investigated these subsets in anti‐neutrophil cytoplasm antibody (ANCA)‐associated vasculitis (AAV) and determined their surface expression of ANCA autoantigens. Flow cytometry was performed on blood from 14 patients with active AAV, 46 patients with AAV in remission and 21 controls. The proportion of classical (CD14^highCD16^neg/low), intermediate (CD14^highCD16^high) and non‐classical (CD14^lowCD16^high) monocytes and surface expression levels of CD14 and CD16 were determined, as well as surface expression of proteinase 3 (PR3) and myeloperoxidase (MPO) on monocyte subsets. There was no change in the proportion of monocytes in each subset in patients with AAV compared with healthy controls. The expression of CD14 on monocytes from patients with active AAV was increased, compared with patients in remission and healthy controls (P < 0·01). Patients with PR3‐ANCA disease in remission also had increased monocyte expression of CD14 compared with controls (P < 0·01); however, levels in patients with MPO‐ANCA disease in remission were lower than active MPO‐ANCA patients, and not significantly different from controls. There was a correlation between CD14 and both PR3 and MPO expression on classical monocytes in AAV patients (r = 0·79, P < 0·0001 and r = 0·42, P < 0·005, respectively). In conclusion, there was an increase in monocyte CD14 expression in active AAV and PR3‐ANCA disease in remission. The correlation of CD14 expression with ANCA autoantigen expression in AAV may reflect cell activation, and warrants further investigation into the potential for increased CD14 expression to trigger disease induction or relapse.     

Reprint of: MicroRNA profiling of human intermediate monocytes

Among the three human monocyte subsets, intermediate CD14++CD16+ monocytes have been characterized as particularly proinflammatory cells in experimental studies and as potential biomarkers of cardiovascular risk in clinical cohorts. To further substantiate the distinct role of intermediate monocytes within human monocyte heterogeneity, we assessed subset-specific expression of miRNAs as central epigenetic regulators of gene expression. We hypothesized that intermediate monocytes have a distinct miRNA profile compared to classical and non-classical monocytes.By using small RNA-seq we analyzed 662 miRNAs in the three monocyte subsets. We identified 38 miRNAs that are differentially expressed in intermediate monocytes compared to both classical and non-classical monocytes with a p value of <10⁻¹⁰, of which two miRNAs – miR-6087 (upregulated) and miR-150-5p (downregulated) – differed in their expression more than ten-fold. Pathway analysis of the 38 differentially expressed miRNAs linked intermediate monocytes to distinct biological processes such as gene regulation, cell differentiation, toll-like receptor signaling as well as antigen processing and presentation. Moreover, differentially expressed miRNAs were connected to those genes that we previously identified as markers of intermediate monocytes.In aggregation, we provide first genome-wide miRNA data in the context of monocyte heterogeneity, which substantiate the concept of monocyte trichotomy in human immunity. The identification of miRNAs that are specific for intermediate monocytes may allow to develop strategies, which particularly target this cell population while sparing the other two subsets.     

MicroRNA profiling of human intermediate monocytes

Among the three human monocyte subsets, intermediate CD14++CD16+ monocytes have been characterized as particularly proinflammatory cells in experimental studies and as potential biomarkers of cardiovascular risk in clinical cohorts. To further substantiate the distinct role of intermediate monocytes within human monocyte heterogeneity, we assessed subset-specific expression of miRNAs as central epigenetic regulators of gene expression. We hypothesized that intermediate monocytes have a distinct miRNA profile compared to classical and non-classical monocytes.By using small RNA-seq we analyzed 662 miRNAs in the three monocyte subsets. We identified 38 miRNAs that are differentially expressed in intermediate monocytes compared to both classical and non-classical monocytes with a p value of <10⁻¹⁰, of which two miRNAs – miR-6087 (upregulated) and miR‐150-5p (downregulated) – differed in their expression more than ten-fold. Pathway analysis of the 38 differentially expressed miRNAs linked intermediate monocytes to distinct biological processes such as gene regulation, cell differentiation, toll-like receptor signaling as well as antigen processing and presentation. Moreover, differentially expressed miRNAs were connected to those genes that we previously identified as markers of intermediate monocytes.In aggregation, we provide first genome-wide miRNA data in the context of monocyte heterogeneity, which substantiate the concept of monocyte trichotomy in human immunity. The identification of miRNAs that are specific for intermediate monocytes may allow to develop strategies, which particularly target this cell population while sparing the other two subsets.     

Monocyte activation in rheumatoid arthritis (RA): increased integrin, Fc gamma and complement receptor expression and the effect of glucocorticoids

The aim of this work was to study the expression of beta 1- and beta 2-integrins, CR1, CD44 and Fc gamma receptors on peripheral blood monocytes in RA. The expression of these receptors was measured by flow cytometry, before and after treatment with low-dose prednisolone. Expression of the same receptors was also measured before and after treatment with metyrapone, a substance that inhibits the synthesis of cortisol in the adrenals. The expression of the beta 2-integrins CD11a, CD11b and CD18, of CD35 (CR1), and of Fc gamma RII and Fc gamma RI (CD32 and CD64) on monocytes was elevated in the RA patients compared with healthy controls, while the expression of the beta 1-integrins (CD29, CD49d, CD49f) was unaffected. A significant correlation between monocyte expression of CD64 and C-reactive protein (CRP), and blood platelet count, respectively, was found in the group of patients with RA. After 4-6 weeks of treatment with low-dose prednisolone, the expression on the monocytes of CD11a, CD11b, CD18, CD35, CD32 and CD64 was normalized. A significant correlation (r = 0.64, P = 0.02) was found between the decrease in expression of CD11b and clinical improvement after prednisolone treatment. Two days of metyrapone treatment, which significantly lowered the serum cortisol levels, elevated the expression of CD35 and CD49f. Priming of peripheral monocytes seems to be one of the mechanisms behind the recruitment of monocytes to the rheumatoid synovium. One reason for the good clinical effects of prednisolone in RA could be a down-regulation of adhesion and phagocytosis receptors on monocytes.     

Human Monocyte Subsets at Homeostasis and Their Perturbation in Numbers and Function in Filarial Infection

To characterize the function and plasticity of the major human circulating monocyte populations and to explore their role in systemic helminth infection, highly purified (by flow-based sorting) human monocyte subsets (CD14^hi/CD16^neg [classical], CD14^{+ or hi}/CD16^med [intermediate], and CD14^neg/CD16^hi [nonclassical]) were examined at homeostasis and after activation. Among these three subsets the classical and intermediate subsets were found to be the major sources of inflammatory and regulatory cytokines, as well as cytokines/chemokines associated with alternative activation, whereas the nonclassical and classical populations demonstrated an ability to transmigrate through endothelial monolayers. Moreover, it was primarily the classical subset that was the most efficient in promoting autologous T cell proliferation. The distribution of these subsets changed in the context of a systemic helminth (Wuchereria bancrofti) infection such that patent infection altered the frequency and distribution of these monocyte subsets with the nonclassical monocytes being expanded (almost 2-fold) in filarial infection. To understand further the filarial/monocyte interface, in vitro modeling demonstrated that the classical subset internalized filarial antigens more efficiently than the other two subsets but that the parasite-driven regulatory cytokine interleukin-10 was exclusively coming from the intermediate subset. Our data suggest that monocyte subsets have a differential function at homeostasis and in response to helminth parasites.     

Different phenotypes of non-classical monocytes associated with systemic inflammation,endothelial alteration and hepatic compromise in patients with dengue

Although dengue can progress to severe stages, the exact causes of this phenomenon are unknown; however, the possibility of monocyte participation is acknowledged. It has been suggested that monocyte subsets (classical, intermediate and non-classical) play differential roles in dengue immunopathology. Therefore, we determined the count of monocyte subsets and obtained the clinical information of patients with dengue. We noted a significant decrease in the count of non-classical monocytes in patients compared with controls. With this finding, we focused on studying the phenotype of non-classical monocytes in the present study. An increase in activation and differentiation markers, such as CD64, CD86, the percentage of tumor necrosis factor-α⁺ cells and exposure of phosphatidylserine, were recorded in the non-classical monocytes of patients compared with controls. Moreover, a significant decrease in the expression of CX3CR1 with a corresponding increase in the expressions of CCR2, CCR5, CD11b and CD54 was detected in the non-classical monocytes of patients in comparison with that of the controls. Significant increases in the frequency of microparticles from endothelium and in the concentrations of interleukin-6 (IL-6), IL-8 and IL-10 were noted in the plasma of patients. These findings demonstrate that in patients with dengue, non-classical monocytes are activated, exhibiting a phenotype associated with more differentiation, produces tumor necrosis factor-α and has a profile of less endothelial surveillance closer to the cellular migration. These changes were associated with hepatic compromise, endothelial alteration and high concentration of circulating cytokines. Hence, alterations of non-classical monocytes seem to be associated with the immunopathology of dengue infection.     

Modulation of monocyte subsets in infectious diseases

Monocytes are effector immune cells but a precise analysis of their role in immune response has been precluded by their heterogeneity. Indeed,human monocytes are composed of at least three different subsets with different phenotypic characteristics and functional properties,the so-called classical,intermediate and nonclassical monocytes. A review of the literature shows that these monocyte subsets are differently affected during viral,bacterial,parasitic and fungal infections.The expansion of the CD16+ compartment(intermediate and non-classical monocytes) is typically observed in the majority of infectious diseases and the increased proportion of CD16+ monocytes is likely related to their activation through their direct interaction with the pathogen or the inflammatory context. In contrast,the number of non-classical and intermediate monocytes is decreased in Q fever endocarditis,suggesting that complex mechanisms govern the equilibrium among monocyte subsets. The measurement of monocyte subsets would be useful in better understanding of the role of monocyte activation in the pathophysiology of infectious diseases.     

蕈样肉芽肿患者外周血单一核细胞CD45RA及CD45RO表达的研究

目的探讨蕈样肉芽肿（Mycosis fungoides,MF）患者外周血单个核细胞CD45RA及CD45RO的表达及其与MF发病的关系。方法应用双荧光抗体标记、流式细胞仪检测15例MF患者外周血单个核细胞CD45RA及CD45RO的表达。结果（1）MF患者外周血CD3^＋、CD3^＋CD8^＋细胞与正常对照比较差异不显著（P〉0.05）。（2）MF患者外周血CD4^＋细胞低于正常对照,差异非常显著（P〈0.001）。（3）MF患者外周血T细胞CD3^＋CD4^＋/CD3^＋CD8^＋比值低于正常对照,差异显著（P〈0.001）。（4）MF患者外周血CD45RA^＋细胞低于正常对照,差异非常显著（P〈0.001）,CD45RO^＋细胞高于正常对照,差异非常显著（P〈0.001）。（5）MF患者外周血CD45RO^＋/CD45RA^＋比值高于正常对照,差异非常显著（P〈0.001）。（6）MF患者外周血CD4^＋CD45RA^＋细胞低于正常对照,差异非常显著（P〈0.001）。（7）MF患者外周血CD4^＋CD45RO^＋细胞及CD8^＋CD45RO^＋细胞均高于正常对照,差异非常显著（均P〈0.001）。（8）MF患者外周血CD4^＋CD45RO^＋/CD4^＋CD45RA^＋比值及CD8^＋CD45RO^＋/CD8^＋CD45RA^＋比值均高于正常对照,差异非常显著（P〈0.01及P〈0.001）。结论MF患者外周血中,不仅存在CD4^＋亚群失调和CD4^＋/CD8^＋比值降低,而且在CD4^＋和CD8^＋亚群中也存在CD45RA^＋、CD45RO^＋亚群失调和CD45RO^＋/CD45RA^＋比值升高,从而导致的机体免疫功能紊乱,可能与MF的发病或病情加剧有关。