中国健康人外周血中具有CD4+CD25nt/hiCD127lo特征的调节性T细胞频率

目的:初步确定健康人外周血中具有CD4+CD25nt/hiCD127lo特征的调节性T细胞(Treg)频率,为临床相关疾病的研究及Treg的分选提供参考.方法:采集312名8～60岁(5个年龄组)、不同性别健康人的静脉血,经三重免疫荧光染色,用流式细胞术分析CD4+CD25nt/hiCD127lo Treg细胞频率,并观察细胞内Foxp3转录因子的表达.结果:健康人CD4+CD25nt/hiCD127lo Treg细胞在外周血中约占CD4+T细胞的(6.55±0.11)%,各年龄组之间有差异(P=0.015),组内性别之间也存在统计学意义(P＜0.05);CD25nt/hiCD127lo细胞特异性地表达Foxp3转录因子.结论:初步确定了中国健康人外周血中具有CD4+CD25nt/hiCD127lo表达特征的细胞频率,为Treg细胞的临床研究奠定了基础;CD25nt/hiCD127lo作为CD4+CD25+Treg细胞表面的特征性标志,可在分选时排除其他细胞干扰,获得较完整的Treg细胞.     

HIV-1感染者CD4+CD25nt/hiCD127lo调节性T细胞PD-1表达水平与疾病进展的关系

目的:阐明HIV-1感染者外周血中具有CD4+CD25nt/hiCD127lo特征的调节性T细胞(Treg)表面PD-1的表达水平与疾病进展的关系.方法:选取108名未经治疗的不同进展期的HIV-1感染者和27名健康人对照, 采集静脉血, 用Ficoll-Hypaque密度梯度离心法分离获得PBMC, 加入PerCP-CD4抗体、 FITC-CD25抗体、 PE-CD127抗体和APC-PD-1抗体, 经细胞表面四色染色、流式细胞术(FCM)分析Treg表面PD-1的表达;另将50 L全血加入Trucount绝对计数管, 采用Multitest CD3/CD8/CD45/CD4试剂盒检测CD4+T细胞绝对数;分离静脉血血浆, NucliSens EasyQ测定血浆HIV-1病毒载量;实验数据采用SPSS14.0 统计学软件分析处理.结果:HIV-1感染者Treg表面PD-1表达水平显著高于健康人(5.33%±2.24% vs 1.72%±0.65%, P<0.01);AIDS期(7.87%±2.23%)明显高于进展期(5.21%±1.72%, P<0.05)和新近感染者(3.22%±1.01%, P<0.05);HIV-1感染者Treg表面PD-1表达水平与血浆中的HIV-1病毒载量和CD4+T细胞绝对数密切相关.结论:首次证实HIV-1感染者外周血中Treg表面PD-1表达增加, 且表达水平与病程进展相关.该结果为进一步揭示HIV-1感染中Treg的效应机制、探索新的免疫治疗方案提供了理论及实验依据.     

卵巢癌患者外周血CD4+CD25hiCD127lo调节性T细胞格局变化及临床意义

目的:观察卵巢癌患者外周血中CD4+CD25hiCD127lo调节性T细胞格局变化及其相关免疫细胞因子TGF-β1、IL-10的变化及与临床病理特征之间的关系,探讨其临床意义.方法:采用流式细胞术(FCM)和酶联免疫吸附法(ELISA)检测70例卵巢癌患者、50例卵巢良性疾患及70例健康者外周血单个细胞中调节性T细胞的比率和血浆TGF-β1、IL-10的水平.结果:①卵巢癌患者外周血中CD4+CD25hiCD127loTreg调节性T细胞占CD4+细胞的比例为6.32%±1.46%(n=70),显著高于卵巢良性疾患4.03%±1.25%(n=50)和健康对照组3.21%±0.96%(n=70),均P＜0.01.术后患者CD4+CD25hiCD127loTreg比率与术前比较无明显差异.②卵巢癌患者血浆中TGF-β1、IL-10水平(256.68±56.34) pg /ml、(28.24±3.12) ng/ml,明显高于良性疾患(156.48±43.68) pg /ml、(20.58±2.39) ng/ml与健康对照组(130.24±35.60) pg/ml、(18.38±2.98) ng/ml,有统计学差异,分别P＜0.001,P＜0.01.③术前卵巢癌患者外周血CD4+CD25hiCD127loTreg比率、血浆中TGF-β1、IL-10水平与患者的临床分期、淋巴结转移以及远处转移有关,P＜0.05～P＜0.001.④相关分析显示,卵巢癌患者外周血 CD4+CD25hiCD127loTreg比率与血浆中TGF-β1水平、IL-10水平呈正相关,r=0.734,P＜0.01;r=0.665,P＜0.01.结论:①CD4+CD25hiCD127loTreg在卵巢癌患者外周血中表达显著增高,这可能是卵巢癌患者免疫功能下降的一个重要原因,并与临床病理特征存在显著相关性;②卵巢癌患者血浆中抑制性细胞因子TGF-β1、IL-10水平明显升高,并与临床病理特征存在显著相关性;③CD4+CD25hiCD127loTreg与TGF-β1、IL-10水平存在正相关,CD4+CD25hiCD127loTreg可能通过产生抑制性细胞因子TGF-β1、IL-10 对效应性T细胞发挥抑制作用.     

HIV感染者外周血CD4+ CD25+ Foxp3+/CD127low/-调节性T细胞表达水平对疾病进展的影响

目的:探讨HIV感染者外周血中CD4+ CD25+Foxp3+调节性T细胞(Treg)、CD4+ CD25+ CD127low/-Treg的水平及其与其他免疫指标的关系.方法:采集68例未经抗HIV治疗的HIV/AIDS患者(长期不进展组即LTNP组29例、典型进展的HIV感染组27例、AIDS组12例)及20例健康成人的外周抗凝全血,经免疫荧光染色,应用流式细胞仪分析CD4+T细胞、CD8+T细胞、NK细胞及CD4+CD25+Foxp3+/CD127low/-Treg的含量,并进行统计学分析.结果:除CD8+T细胞外,HIV/AIDS患者外周血中CD4+T细胞、NK细胞、CD4 +/CD8+结果均明显低于健康对照组(P＜0.05);随着疾病的进展,LTNP组、HIV组、AIDS组CD4+T细胞百分比、绝对值计数,CD8+T细胞绝对计数,NK细胞绝对计数,CD4 +/CD8+比值逐渐下降,而CD8+T细胞百分比逐渐上升.对CD4+ CD25+ Foxp3+ Treg与CD4+ CD25+CD127low/-Treg百分含量、绝对计数进行多重比较发现,各组间CD4+ CD25+ Foxp3+ Treg与CD4-CD25+ CD127low/-Treg所占CD4+T细胞百分含量的差异均有统计学意义(P＜0.05),并且随着疾病的发展,CD4+ CD25+ Foxp3+/CD127low/ Treg细胞百分含量逐渐上升,LTNP组与健康对照组之间、HIV组和AIDS组之间CD4+ CD25+Foxp3+/CD127low/ Treg绝对计数差异无统计学意义(P＞0.05),其余各组间的差异均有统计学意义(P＜0.05),并且随着疾病的发展,CD4+ CD25+ Foxp3-/CD127low/-Treg绝对计数逐渐下降.结论:CD4+ CD25+ Foxp3 +/CD127low/-Treg在HIV持续感染的免疫发病机制中有一定作用.     

HIV/AIDS患者疾病进程与CD4+CD25hi调节性T细胞之间相关性研究

目的 通过分析不同阶段HIV感染者外周血CD4+CD25hi调节性T细胞(CD4+CD25hiregulatory T cells,Treg cells)与外周血免疫状态和病毒载量的相关性,探讨Treg细胞对HIV/AIDS发病进程的影响.方法 采集116例HIV感染者和21例正常人对照外周血,用4色流式细胞术进行CD4+和CD8+T细胞绝对数计数;用3色流式细胞术进行Treg细胞测定;用荧光定量PCR法进行HIVRNA载晕测定.实验数据用回归统计学方法和T检验方法进行分析.结果 HIV感染者外周血Treg细胞频率在HIV感染初期显著下降,之后随着疾病的进程逐渐升高.在CD4+T细胞大于300/μl的患者低于正常对照组,在CD4+T细胞小于100/μl的患者高于正常对照组,差异具有统计学意义.Treg细胞频率与CD4+T淋巴细胞绝对数和CD4+/CD8+之间均呈负相关.其相关系数r和P值各为r=-0.564,P＜0.001和r=-0.377,P＜0.001;Treg细胞频率与血浆HIV病毒载量呈正相关,其相关系数r=0.514.P＜0.001.结论 CD4+CD25hi Treg细胞可能是参与艾滋病免疫发病机理的重要细胞,在HIV感染发病进程的不同阶段具有不同的意义,其确切机制有待进行进一步研究.     

强直性脊柱炎患者外周血CD4+调节性T细胞的变化及意义

目的 探讨强直性脊柱炎(ankylosing spondylitis,AS)患者外周血中CD4+调节性T细胞(regulatory T cells,Treg)的表达、功能及意义.方法 采用流式细胞术检测78例AS患者和50例健康志愿者外周血中CD4+CD25+CD127lo/- Treg、细胞毒性T细胞(cytotoxic T lymphocytes,CTL)和NK细胞,采用ELISA法检测血清中β型转化生长因子(transforming growth factor-β,TGF-β)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的表达水平.从患者外周血单个核细胞中磁珠分选出CD4+CD25+ Treg细胞,混合淋巴细胞培养(mixed lymphocyte culture, MLC)分析其免疫抑制功能.结果 AS活动期患者外周血中CD4+CD25+CD127lo/-Treg占CD4+ T淋巴细胞的百分比为(4.36±1.21)%,MLC中CD4+CD25+ Treg抑制同种异体T淋巴细胞增殖功能低下,与其Treg分泌TGF-β减少相关,CD4+ Treg含量及功能均低于健康志愿者(P<0.05).AS患者外周血中CD4+CD25+CD127lo/- Treg水平与TGF-β呈正相关,与TNF-α呈负相关.结论 AS患者外周血中Treg表达水平低,且存在功能缺陷,导致体内诱导免疫耐受机能不足,可能参与AS免疫发病.     

慢性乙型肝炎患者外周血中CD4+CD25+调节性T细胞的变化和意义

目的 观察慢性乙型肝炎感染者外周血CD4 CD25 调节性T细胞(Treg)的频率,特征性表型及与临床指标的相关性.方法 采集44例慢性乙型肝炎,29例健康人外周血,多色流式分析Treg的频率,CD4 CD25 Foxp3 调节性T细胞的频率.所有病例均经酶联免疫吸附实验(ELISA)检测HBsAg、HBsAb、HBeAg、HBeAb和HBcAb,实时荧光定量RT-PCR检测血清HBV DNA载量及肝功能的检测.结果 慢性乙型肝炎组Treg的频率(5.02%±2.07%)显著高于正常对照组(3.35%±1.51%,P＜0.05);Foxp3在Treg上特异性表达,慢性乙型肝炎组CD4 CD25 Foxp3 调节性T细胞的频率(2.05%±1.03%)显著高于正常对照组(1.30%±0.68%,P＜0.05);慢性乙型肝炎组Treg的频率与病毒载量呈正相关.结论 Treg在慢性乙型肝炎感染者中明显增高,并与病毒载量相关,提示Treg在慢性乙型肝炎中担负着重要的免疫调节作用,可能是造成乙肝病毒感染慢性化的重要因素.     

乙型肝炎病毒感染者外周血CD4+T细胞CD25、CD127不同亚群表达的检测及临床意义

目的 研究乙型肝炎病毒(HBV)感染者外周血CD4+T细胞表面CD25、CD127不同亚群的表达情况及临床意义。方法 用荧光抗体CD127-FITC、CD4-PECY5、CD25-PE标记T细胞。用流式细胞仪分别测定53例慢性乙型肝炎患者和53例HBV携带者CD4+T细胞表面CD25、CD127不同亚群的表达情况。对20例HBV-DNA阳性乙型肝炎病毒感染者干扰素治疗进行随访。结果与健康对照组[7.26％(6.15％,8.50％)]比较,慢性乙型肝炎患者[11.23％(9.10％,14.86％)]、HBV携带者[13.34％( 10.73％,18.90％)]CD25-CD 127-均显著升高,差异均有统计学意义(Q=4.559,P＜0.05;Q=6.230,尸＜0.05)。慢性乙型肝炎患者CD25hiCD127low/-[8.78％ (7.62％,10.44％)]显著高于健康对照[6.76％(5.73％,8.23％)]和HBV携带者[6.99％(5.77％,9.34％)],差异均有统计学意义(Q=3.497,P＜0.05;Q=3.103,P＜0.05)。HBV-DNA阳性组CD25-CD127-显著低于阴性组,两者差异有统计学意义[(12.92±5.20)％比(15.78±6.91)％,t=2.290,P=0.024],而CD25+/-CD127+显著高于阴性组,两者差异有统计学意义[(79.27±5.20)％比(76.02±7.04)％,t=2.194,P=0.030]。与治疗前比较,干扰素治疗12周CD25hiCD127low/-显著升高[(9.29±2.51)％比(11.08±2.38)％,t=2.820,P=0.011],而CD4+CD25-CD127-显著降低,两者差异有统计学意义[(13.86±5.72)％比( 10.86±3.60)％,t=2.469,P=0.024]。结论 HBV感染者外周血CD4+T细胞中CD25-CD127-亚群的表达与病毒的感染和清除有关;CD25hiCD 127low/-亚群的表达升高与发病有关。外源性干扰素可升高CD25hiCD127low/-的表达,降低CD25-CD127-的表达,从而抑制免疫反应。     

CD4+ CD25+调节性T细胞在HIV/AIDS患者中的作用及其与HIV病毒载量的相关性研究

目的 研究HIV感染者／AIDS患者外周血CD4^＋ CD25^＋ 调节性T细胞（CD4^＋ CD25^＋ regulatory Tcell，Treg）频率、功能及其临床意义。方法 选择31例HIV感染者／AIDS患者和30例健康对照者，采用流式细胞仪检测各组外周血Treg的表型和频率。采取MACS磁珠分选CD4^＋CD25^＋T细胞，利用[^3H]胸腺嘧啶掺入法检测CD4^＋ CD25^＋T细胞在特异性HIV抗原刺激下对CD4^＋ CD25-T细胞的增殖影响。结果HIV／AIDS患者组与正常对照组相比较，外周血CD4^＋ CD25^＋ T细胞频率在统计学上差异无统计学意义。与正常对照组比较，HIV感染者外周血CD4^＋ CD25^＋ T细胞频率升高，差异有统计学意义（P〈0.01）；与正常对照组比较，AIDS患者者外周血CD4^＋ CD25^＋ T细胞频率降低，差异有统计学意义（P〈0．0001）。HIV RNA病毒载量与患者外周血CD4^＋ CD25^＋ T细胞数量呈正相关性（P〈0．01）。CD4^＋ CD25^＋ T细胞具有抑制HIV特异性的CD4^＋ CD25^- T细胞的增殖作用。结论HIV感染者／AIDS患者的细胞免疫功能紊乱，CD4^＋ CD25^＋ T细胞能抑制HIV感染者／AIDS患者的HIV特异性细胞免疫反应，促进HIV病毒复制，与形成持续HIV感染有关。     

中国健康人外周血中具有CD4+CD25nt/hiCD127lo特征的调节性T细胞频率

目的：初步确定健康人外周血中具有CD4^＋ CD25^nt/hi CD127^lo特征的调节性T细胞（Treg）频率，为临床相关疾病的研究及Treg的分选提供参考。方法：采集312名8—60岁（5个年龄组）、不同性别健康人的静脉血，经三重免疫荧光染色，用流式细胞术分析CD4^＋ CD25^nt/hi CD127^lo Treg细胞频率，并观察细胞内Foxp3转录因子的表达。结果：健康人CD4^＋ CD25^nt/hi CD127^lo Treg细胞在外周血中约占CD4^＋ T细胞的（6．55±0．11）％，各年龄组之间有差异（P=0．015），组内性别之间也存在统计学意义（P〈0．05）； CD25^nt/hi CD127^lo细胞特异性地表达Foxp3转录因子。结论：初步确定了中国健康人外周血中具有CD4^＋ CD25^nt/hi CD127^lo表达特征的细胞频率，为Treg细胞的临床研究奠定了基础； CD25^nt/hi CD127^lo作为CD4^＋ CD25^＋ Treg细胞表面的特征性标志，可在分选时排除其他细胞干扰，获得较完整的Treg细胞。     

CD70 represents the human ligand for CD27

The recently identified CD27 ligand (L) Is a type II transmembranemolecule with significant structural homology to tumor necrosisfactor (TNF)-, TNF-ß, lymphotoxin ß, CO40L,and CD30L. Using a CD27L specific mAb we examined the tissuedistribution of the molecule, and found Its expression to berestricted to B cells in occasional germinal centers, stromalcells in the thymic medulla, and scattered T cells in tonsils,skin and gut. As the limited expression of CD27L closely resembledthe reported distribution of the activation antigen CD70, wetested whether CD70 represents the human CD27L. CD70 mAb werefound to react with CD27L-expressing transfected mouse fibroblasts.Moreover a number of CD70 mAb could specifically interfere withthe cellular binding of CD27L mAb. Thus, CD70 Is Identical tothe human CD27L.     

Signals through CD8 or CD4 can induce commitment to the CD4 lineage in the thymus

Differentiation of thymocytes into mature single-positive T cells is an ordered process involving sequential interactions between T cell receptor (TCR), coreceptors (CD4 or CD8) and their appropriate major histocompatibility complex-encoded ligands. Precisely how these receptor/co-receptor engagements determine lineage commitment is still controversial, but recently it has been suggested that quantitative differences in the signal transmitted by coligation of CD4 versus CD8 with TCR might provide the discriminating signal. We examine this hypothesis, using bispecific F(ab')₂ antibodies to mimic TCR/co-receptor engagement during thymocyte differentiation. These bispecific antibodies lack Fc and can engage surface molecules without extensive cross-linking or targeting to Fc receptor-bearing cells. We show that TCR/CD3 co-ligation with CD4 induces efficient differentiation of mature CD4 lineage cells, irrespective of their TCR specificity. Interestingly, TCR/CD3 co-ligation with CD8 also induces maturation of CD4T cells, although less efficiently, but not of CD8 T cells. Thus, although the signals delivered by co-ligation of TCR and CD8 appear weaker than from co-ligation of TCR and CD4, the outcome from either engagement is the same. These data suggest that differences in signal intensity alone do not determine lineage commitment in the thymus, but that distinct signals are required for CD4 and CD8 single-positive cell differentiation.     

CD8 lethargy in the absence of CD4 help

CD4 T cell help was proposed to have a pivotal role in orienting CD8 T cell responses to antigen stimulation. By activating antigen-presenting cells (APC), CD4 cells would induce their expression of costimulatory molecules, the "signal two" required to induce full CD8 activation, preventing CD8 tolerance. Recent data on this subject is contradictory, as the absence of help did not always result in CD8 tolerance. These differences were attributed either to the presence of residual CD4 help or, respectively to the type of antigen stimulation, the peptide affinity, the CTL frequencies, and/or the strength of the response. We therefore reassessed the role of CD4 help in CD8 responses using a system where CD4 cells are absent and APC not activated. This system can be manipulated to induce CD8 tolerance (at high antigen concentrations) or CD8 memory (at low antigen concentrations). We found that the presence of CD4 help did not prevent tolerance induction. On the other hand, the absence of CD4 help did not induce CD8 tolerance, but rather led to differentiation stage intermediate between naive/memory/tolerant cells that we call "lethargy". These findings indicate that role of CD4 help in CD8 responses does not follow a simple on-off rule, as previously suggested. They also reveal that the "tolerance versus memory" dichotomy fails to account for all possible states/properties of antigen-experienced CD8 cells. Depending on the priming conditions, other intermediate stages of differentiation may occur.     

CD4 and CD8: hogging all the Lck

Specificity of T cell receptors (TCRs) to major histocompatibility complex (MHC) might be intrinsic or imposed by thymic selection. Van Laethem et al. (2007) propose that the sequestration of the kinase Lck by coreceptors prevents the selection of non-MHC-reactive TCRs.     

CD4+CD45R+ cells are preferentially activated through the CD2 pathway

CD4 cell subsets, CD4+CD45R+ (CDw29-) cells and CD4+CD45R- (CDw29+) cells, can be differently triggered by various stimuli and possess distinct functions. In the present study, cell activation in CD4+CD45R+ and CD4+CD45R- subsets mediated by CD3-Ti antigen-receptor complex or CD2 molecule were examined by using anti-CD3 antibody or pairs of anti-CD2 antibodies (anti-T11(2) and anti-T11(3) antibodies). The results showed that CD4+CD45R+ cells were preferentially activated through the CD2 pathway, whereas both subsets were equally activated through the CD3-Ti antigen-receptor pathway when a second signal such as monocytes or interleukin 2 was present. The different responsiveness of CD4+CD45R+ and CD4+CD45R- subsets through the CD2 molecule did not appear to be due to differences in the distribution or number of T11(2) and T11(3) determinants. These data suggest that some part of the functional diversity of CD4 cell subsets might be explained by the differences in cell activation through the CD2 molecule.     

B cells in the aged: CD27, CD5, and CD40 expression

Ageing is characterized by numerous changes in lymphocyte subpopulations. In the present paper we have focused on B cells carrying the surface markers CD27, CD5 and CD40. CD27 is considered a marker of primed (memory) cells and its engagement promotes the differentiation of memory B cells into plasma cells. CD5 is expressed on B1 cells, which are considered to be responsible for T cell-independent antibody production other than autoantibodies. The CD40 molecule binds CD40L (CD154) and is necessary for T-dependent antibody responses. Here we show that the absolute number of CD5+ and CD40+ B cells is decreased in the elderly, while CD27+ B lymphocytes only marginally decrease in centenarians. However, there is a decrease of the percentage of CD5+ B cells, an increase of CD27+ B cells, while CD40 does not change significantly. These data, together with the increased number of NK cells during aging, suggest different regulation of antibody production in the elderly which might be another example of immune remodeling with aging, based on interactions between human B and NK cells.     

Co-cultivation of CD4+ and CD8+ human T-cells leads to the appearance of CD4 cells expressing CD8 through de novo synthesis of the CD8 alpha-subunit

The appearance of a population of dual-staining CD4+CD8+ cells in human T-lymphocyte cultures has been reported by various authors, including our own observation that they are always seen in simple phytohaemagglutinin-stimulated cultures from several different donors. The purpose of the present study was to investigate factors involved in the dual-staining (DS) phenotype, and to clarify some apparent inconsistencies between published observations. Our findings can be summarised as follows. 1. A population of DS CD4+CD8+ cells always appears in PHA-stimulated T-cell cultures if they contain both CD4 and CD8 subsets. The incidence of DS cells is related to PHA concentration, but other factors are involved since DS cells are not seen in PHA-stimulated cultures of purified CD4+ or CD8+ cells. Stimulation with PHA is not a prerequisite since very similar results are seen with ConA. 2. Direct physical contact between CD4+ and CD8+ cells is required for the appearance of the DS phenotype; soluble factors alone, including IL-4, appear nor to be responsible. 3. The DS phenotype in these conditions is always CD4+ cells weakly expressing CD8 and is a consequence of de novo synthesis of the CD8alpha molecule by the CD4+ cells.     

Competition controls the rate of transition between the peripheral pools of CD4+CD25- and CD4+CD25+ T cells

Recent reports have hinted that it is possible to regenerate CD4+CD25+ regulatory T cells (Treg) from CD4+CD25- cells, a phenomenon termed conversion. We evaluated the relative contribution of this process to the Treg pool by transferring purified populations of CD4+ T cells into T cell-deficient mice. We report that conversion of CD25- cells into the CD4+CD25+Treg pool is minor if other bona fide CD25+ Tregs are present. Moreover, in the same hosts, the loss of CD25 expression by a population of Tregs also decreases in the presence of co-injected CD4+CD25- cells. Thus, the rate of exchange between CD25- and CD25+ T-cell populations is determined by the presence or absence of T-cell competitors. Our results attest for the role of competition in the contribution of different T-cell subsets for the regeneration of the peripheral CD4+ T-cell pool during lymphopenia.     

广东HIV/AIDS患者舌象分析及其与CD4、CD8、CD4/CD8计数的相关性研究

目的分析广东HIV/AIDS患者的舌象规律及其与CD4、CD8、CD4/CD8计数的规律。方法对609例广东HIV/AIDS患者进行舌象分析和CD4、CD8T淋巴细胞检测,探讨其相关性。结果HIV/AIDS患者CD4、CD4/CD8比值均低于正常水平;两组淡红舌患者的CD4、CD4/CD8比值均高于其他4种舌色(淡白舌、红舌、暗舌、紫舌)(P<0.05);两组淡白舌患者的CD4、CD4/CD8比值均低于其他4种舌色(P<0.05);HIV/AIDS患者暗舌的比例(41.38%)均大于其他舌色,其次是红舌(35.47%)(P<0.05);HIV/AIDS患者以白腻苔(44.83%)为主,其次为黄腻苔(26.11%)、薄白苔(20.20%),少苔(3.45%)。结论舌象能客观反映HIV/AIDS患者身体免疫机能;广东HIV/AIDS患者多出现正气虚,夹瘀、夹痰化热的表现。