CD3~+、CD4~+、CD8~+T细胞水平在胃癌患者外周血中的变化

目的探讨T淋巴细胞亚群CD3+、CD4+、CD8+和CD4+/CD8+比值水平在胃癌患者外周血中的表达及意义。方法采用血液分析仪技术,检测40例胃癌手术前患者(按临床分期为Ⅰ～Ⅱ级组18例,Ⅲ～Ⅳ级组22例)及25名正常对照组外周血CD3+、CD4+、CD8+细胞和CD4+/CD8+比值T细胞水平。结果胃癌患者外周血CD3+、CD4+细胞、CD4+/CD8+比值分别为0.78%±0.35%、0.37%±0.21%、0.61%±0.42%,明显低于正常对照组(P<0.05);胃癌Ⅲ～Ⅳ级组CD3+、CD4+细胞CD4+/CD8+比值分别为0.42%±0.27%、0.21%±0.17%、0.29%±0.25%,明显低于Ⅰ～Ⅱ级组(0.95%±0.35%、0.45%±0.19%、0.76%±0.30%,P<0.05)。结论检测胃癌患者手术前外周血CD3+、CD4+、CD8+细胞和CD4+/CD8+比值T细胞水平,可以初步评估胃癌患者机体免疫状态,也为肿瘤的免疫增强治疗提供了理论依据。     

CD4^+/CD8^+比值异常系统性红斑狼疮患者PD-L1和IFN-α血清水平检测及其临床意义

目的:通过检测CD4^+/CD8^+比值异常的系统性红斑狼疮(systemic lupus erythematosus,SLE)患者血清程序性凋亡受体配体1(programmed cell death ligand 1,PD-L1)和α-干扰素(interferon-α,IFN-α)水平,探讨PD-L1和IFN-α与SLE患者CD4^+/CD8^+比值异常的关系。方法:73例SLE患者以CD4^+/CD8^+参考范围(1.5~2.5)为标准,分为CD4^+/CD8^+倒置组(29例),CD4^+/CD8^+升高组(17)例,CD4^+/CD8^+正常组(27例),另选取20位健康体检者为健康对照组;采用流式细胞术检测SLE患者CD3^+C D 4^+和CD3^+CD8^+T细胞,ELISA法检测血清PD-L1,IFN-α和抗dsDNA抗体水平,分析PD-L1,IFN-α与抗dsDNA抗体的相关性。结果:CD4^+/CD8^+倒置和升高组补体C3和C4水平显著低于其余二组(均P<0.01)。CD4^+/CD8^+倒置和升高组C-反应蛋白(C-reactive protein,CRP)水平显著高于正常组和健康组(均P<0.01),而升高组CRP水平显著高于倒置组(P<0.01)。CD4^+/CD8^+倒置及升高组SLE患者抗dsDNA抗体滴度、SLE疾病活动度评分(SLE disease activity index,SLEDAI)明显高于正常和健康组(均P<0.01)。CD4^+/CD8^+倒置和升高组PD-L1,IFN-α水平均显著高于健康组(均P<0.05);倒置组PD-L1,IFN-α水平均显著高于正常组,而升高组IFN-α与正常组差异无统计学意义(P>0.05)。CD4^+/CD8^+倒置和升高组SLE患者血清PD-L1和IFN-α均与抗dsDNA抗体滴度成正相关(均P<0.01)。CD4^+/CD 8^+异常组SLE患者病原体感染率显著高于其余二组(均P<0.01)。结论:病原体感染是SLE患者CD4^+/CD8^+比值异常的直接原因,CD4^+/CD8^+异常SLE患者血清PD-L1和IFN-α水平均升高且与抗dsDNA抗体呈正相关,提示PD-L1和IFN-α调节T细胞活化共同参与免疫过程。     

反复呼吸道感染儿童吸入重组人干扰素α1b后临床疗效和血CD4+、CD4+/CD8+比值变化

目的 研究反复呼吸道感染儿童吸入重组人干扰素α1b后临床疗效和血CD4+、CD4+/CD8+比值的变化.方法 以100例确诊反复呼吸道感染儿童为研究对象,随机分为观察组50例,对照组50例.两组分别于治疗前后行流式细胞术检测血CD4+、CD4+/CD8+比值的比率.结果 治疗前两组患儿血CD4+、CD4+/CD8+比值比较差异无统计学意义(P均＞0.05),治疗后两组患儿血CD4+、CD4+/CD8+比值比较差异有统计学意义(P均＜0.01);观察组治疗前后血CD4+、CD4+/CD8+比值比较差异有统计学意义(P均＜0.01);治疗组总有效率明显大于对照组,差异有统计学意义(X2=6.78,P ＜0.05).结论 吸入重组人干扰素α1b可使血CD4+、CD4+/CD8+比值升高,增强T淋巴细胞的功能,治疗儿童反复呼吸道感染.     

复方苦参注射液在乳腺癌术后辅助化疗患者中的应用

目的：探究复方苦参注射液在乳腺癌（BC）术后辅助化疗患者中的应用及对CD4+、CD8+T细胞比值（CD4+/CD8+）的影响。方法：选取医院2017年4月至2019年4月收治的116例BC患者为研究对象,随机分为观察组与对照组,各58例。对照组予以氟尿嘧啶、表阿霉素及环磷酰胺（FEC）方案进行化疗;观察组在对照组基础上予以复方苦参注射液联合治疗。比较两组临床疗效;比较两组治疗前与治疗18周后细胞亚群水平[CD3+、CD4+/CD8+、自然杀伤细胞（NK）];比较两组白细胞（WBC）、血小板（PLT）及白细胞介素-2（IL-2）、白细胞介素-6（IL-6）水平;比较两组化疗毒副反应发生情况。结果：观察组治疗总有效率明显高于对照组（P＜0.05）;治疗18周后,两组CD3+、CD4+/CD8+、NK水平均较治疗前升高,且观察组高于对照组,但CD3+水平较治疗前升高不明显,差异无统计学意义（P＞0.05）,观察组CD4+/CD8+、NK水平均明显高于对照组,差异有统计学意义（P＜0.05）;治疗18周后,两组WBC、PLT、IL-6水平均较治疗前降低,观察组IL-6水平低于对照组,但WBC、PLT水平高于对照组,两组IL-2水平均较治疗前显著升高,且观察组高于对照组（P＜0.05）;治疗过程中,观察组化疗毒副反应发生率较对照组低（P＜0.05）。结论：复方苦参注射液应用于BC术后化疗患者中可获得良好疗效,其免疫功能得以改善,且能减少化疗毒副反应发生,在临床辅助BC术后化疗有重要意义。     

登革热患者外周血CD4+、CD8+T细胞及IL-10的检测分析

目的:观察登革热患者外周血CD4+、CD8+T细胞及白介素-10(IL-10)的变化,探讨其在登革热疾病的发生和发展中的作用.方法:12例健康人和18例登革热患者于治疗前后采静脉血,采用流式细胞仪检测CD4+、CD8+T细胞并计算CD4+/CD8+比值,ELISA法检测血清IL-10水平,同时作外周血白细胞、血小板计数.结果:与正常健康人和治疗后相比,登革热患者治疗前外周血CD4+细胞百分比、CD4+/CD8+比值明显降低(P＜0.01),CD8+细胞百分比和血清IL-10显著增高(P＜0.01),白细胞、血小板计数均明显下降(P＜0.01);治疗后患者以上指标均与健康人无明显差异.结论:CD4+、CD8+T细胞在登革热病毒感染后异常激活,CD4+/CD8+比值明显降低,IL-10分泌增高,可能在登革热的发病中起重要作用.     

超声刀和电刀对胃癌患者手术前后免疫功能及应激的影响

目的 探讨超声刀和电刀对胃癌根治术后免疫功能和术后应激的影响.方法 前瞻性分析63例胃癌改良根治术患者资料,其中35例使用超声刀,28例用电刀,比较两组淋巴结清扫时间、术中出血量、术后72 h引流量情况,应用流式细胞仪测定两组术后外周血中T淋巴细胞亚群CD3+、CD4+、CD8+、CD4+/CD8+比率,术后第2天检测血白细胞计数、粒细胞百分比、C反应蛋白、血糖.结果 超声刀组与电刀组相比,CD3+、CD4+、CD8+、CD4+/CD8+比率,血糖无明显差异(P>0.05);对比术中出血量、淋巴结清扫时间、术后72 h引流量、白细胞计数、粒细胞百分比、C反应蛋白,超声刀组均有明显减少(P<0.05或P<0.01).结论 两种工具在胃癌根治术中切除效果及对术后免疫功能影响无明显差异,但应用超声刀术后恢复快且对术后应激反应小.     

CD64指数与败血症患者调节性T细胞的相关性分析临床研究

目的通过观察CD4+CD+/highCD127low/-、CD14+人类白细胞抗原(HLA-DR)+以及CD64的指数来探究败血症患者的临床治疗方法。方法回顾性分析102例败血症患者的临床资料,将其列为治疗组,另选87例健康人作为对照组,分别观察两个组别CD4+CD+/highCD127low/-、CD14+HLA-DR+与CD64的指数,再详细记录白细胞计数(WBC)与C反应蛋白(CRP)的水平,观察持续1个月,并对两组进行对比分析。结果治疗组的CD4+CD+/highCD127low/-、及CD64的平均指数以及CRP、WCB水平均明显低于对照组,且CD14+HLA-DR+的平均指数明显高于对照组,差异有显著性(P<0.05)。结论研究观察CD4+CD+/highCD127low/-、CD14+HLA-DR+以及CD64的指数对临床治疗败血症有指导意义。     

局部灌注治疗重症急性胰腺炎感染临床疗效分析

目的探讨局部灌注治疗重症急性胰腺炎(severe acute pancreatitis,SAP)感染的临床疗效。方法我院ICU接受治疗的SAP感染患者82例,按照随机数字表法分为局部灌注组和全身组各41例。全身组行常规治疗+药物全身治疗,局部灌注组予常规治疗+局部灌注治疗。观察两组血糖、血淀粉酶(AMY)、谷丙转氨酶(ALT)、血肌酐(Scr)、胰高血糖素;血清C反应蛋白(CRP)、肿瘤坏死因子(TNF-α)、血清白介素-6(IL-6)、白介素-1β(IL-1β)等炎性因子;血清CD3~+、CD4~+、CD8~+、CD4~+/CD8~+等T细胞水平。结果治疗后局部灌注组血糖、AMY、ALT、Scr、胰高血糖素水平,血清IL-6、IL-1β、TNF-α、CRP、CD8~+水平均低于全身组,血清CD3~+、CD4~+、CD4~+/CD8~+水平均高于全身组,总有效率高于全身组(P0.05)。结论局部灌注治疗SAP感染可有效改善肝肾功能,清除炎性因子,纠正免疫失衡,疗效显著。     

替罗非班对急性脑梗死患者神经功能损伤及炎症介质、免疫功能的影响研究

目的：替罗非班对急性脑梗死患者神经功能损伤及炎症介质、免疫功能的影响研究。方法：将2019年1月~2020年12月进行急性脑梗死住院治疗的76例患者随机分为观察组和对照组,每组38例。对照组使用阿司匹林+氢氯吡格雷治疗,观察组在对照组基础上联合使用替罗非班治疗。比较两组炎症介质、神经功能、免疫功能。结果：观察组肿瘤坏死因子-α、白介素-6、C反应蛋白低于对照组;观察组神经功能评分低于对照组;观察组CD4+、CD4+/CD8+水平高于对照组,C3、C4水平低于对照组（P＜0.05）。结论：替罗非班能够改善急性脑梗死患者的神经功能,降低炎症介质水平,提高机体免疫功能。     

脐血IL-4、CD4+、CD8+、CD4+/CD8+与乙型肝炎病毒宫内感染的相关性

目的了解新生儿脐血IL-4、CD4+、CD8+CD4+/CD8+与乙型肝炎病毒(HBV)宫内感染的关联性,为早期发现新生儿感染HBV提供帮助。方法选择HBV感染的孕妇分娩的新生儿75例作为研究组,根据定性测得的乙肝两对半如乙肝表面抗原(HBSAg)、乙肝表面抗体(抗-HBS)、e抗原(HBeAg)、e抗体(抗-HBe)、核心抗体(抗-HBC)结果和定量测得的HBV-DNA值结果将研究组分为HBV宫内感染组17例,非宫内感染58例;并随机选择同一时间段内体检未发现异常的孕妇娩出的新生儿43例作为对照组,并使用不同的方法如酶联免疫吸附测定(ELISA)法检测IL-4水平、流式细胞术检测研究指标CD4+、CD8+、CD4+/CD8+各数值水平。分析3组新生儿脐血IL-4、CD4+、CD8+、CD4+/CD8+与HBV宫内感染的的相关性。结果 3组新生儿进行两两比较,宫内感染组脐血IL-4、CD4+、CD8+、CD4+/CD8+与非宫内感染组相比,宫内感染组新生儿脐血II-4、CD4+、CD8+、CD4+/CD8+与对照组相比,差异均有统计学意义(均P0.05),而非宫内感染组新生儿脐血IL-4、CD4+、CD8+、CD4+/CD8+与对照组比较,差异均无统计学意义(均P0.05)。宫内感染组新生儿IL-4、CD8+明显高于非宫内感染组,CD4+、CD4+/CD8+明显低于非宫内感染组,差异均有统计学意义(均P0.05)。结论 HBV感染的孕妇分娩的新生儿脐静脉血IL-4水平升高,CD4+T细胞因子下降,CD8+T细胞因子升高,CD4+/CD8+比值下降,均有助于HBV宫内感染的早期发现和诊断。     

全T细胞相关抗原在非特殊类型外周T细胞淋巴瘤中的表达及其诊断意义

目的 观察CD2、CD3、CD5、CD7在非特殊类型外周T细胞淋巴瘤（PTL-U）和淋巴组织反应性增生（RLM）中的表达情况，探讨其在T细胞增生性病变良、恶性诊断中的辅助价值。方法 应用免疫组化EnVision法检测22例PTL-U和11例RLH中CD2、CD3、CD5、CD7的表达。结果 22例PTL-U中18例（81.8％）存在一种或几种抗原不表达，其中12例仅CD7（-），3例CD5（-），1例CD2（-），1例CD3和CD5（-），1例CD3、CD5和CD7（-）。在RLH病例中仅1例CD7表达数量少于CD2、CD3、CD5，其余10例CD2、CD3、CD5、CD7滤泡外阳性形式和数量大致相等。结论 对于T细胞增生性病变，在形态学鉴别良、恶性困难时，可以通过CD2、CD3、CD5、CD7染色观察是否有部分抗原丢失作为诊断PTL-U的参考指标。     

All for CD91 and CD91 for all

Heat shock proteins interact with antigen-presenting cells through their receptor, CD91, eliciting a cascade of events including maturation, activation and representation of chaperoned foreign peptides with class I molecules on their surface. In turn, this facilitates recognition of non-self leading to induction of a cytotoxic T cell response. The abundance of heat shock proteins in tumours and their presence in virion coats makes them attractive propositions for use in antitumour and antiviral strategies.     

Tyrosine phosphorylation of CD6 by stimulation of CD3: augmentation by the CD4 and CD2 coreceptors

When T cells are activated via the T cell receptor (TCR) complex a number of cellular substrates, including some cell surface proteins, become phosphorylated on tyrosine (Tyr) residues. Phosphorylation of cytoplasmic Tyr renders these cell surface receptors competent to interact with proteins that link cell surface receptors to protein in the intracellular signaling pathways. Here we show that Tyr residues in the cytoplasmic domain of CD6 become phosphorylated upon T cell activation via the TCR complex. Tyr phosphorylation was observed when the T cells were activated by crosslinking CD3 or by cocrosslinking CD3 with CD2 or CD4, but not when the cells were stimulated by crosslinking CD2, CD4, or CD28 alone. Unlike other Tyr kinase substrates, such as the phospholipase C gamma 1-associated pp35/36 protein, whose level of Tyr phosphorylation is highest when T cells are activated by cocrosslinking CD3 with CD2, the levels of CD6 Tyr phosphorylation are highest when T cells were activated by cocrosslinking CD3 with CD4.     

CD137 enhances cytotoxicity of CD3CD56 cells and their capacities to induce CD4 Th1 responses

CD137 (4-1BB) is a TNFR superfamily member that mediates the costimulatory signal resulting in T cells and NK cells proliferation and cytokines production, but the effects of CD137 signaling on CD3⁺CD56⁺ cell subpopulation have not been well-documented. The aim of this study was to investigate the effects of CD137 signaling on regulation of CD3⁺CD56⁺ cell function. Anti-CD137 mAb or mouse IgG1 isotype control was added to CIK cell culture to determine the effects of proliferation and anti-tumor effects on CD3⁺CD56⁺ cells. We observed that anti-CD137 mAb could dramatically promote proliferation of CIK cells. And CD137–CIK cells and CD3⁺CD56⁺ cell subpopulation within them possessed higher ability to kill tumor cell line A549. The SCID mice engrafted with A549 cells and treated with CD137–CIK cells have prolonged survival. Further studies revealed that the percentages of CD3⁺CD56⁺ cells were elevated significantly in CD137–CIK cells. The expression of NKG2D was up-regulated on CD3⁺CD56⁺ cells from CD137–CIK cells. The expression of IFN-γ, IL-2 and TNF-α increased significantly whereas the production of TGF-β₁, IL-4 and IL-10 decreased in CD3⁺CD56⁺ cells from CD137–CIK cells. In addition, anti-CD137 mAb can elevate the capacity of CD3⁺CD56⁺ cells to induce CD4⁺ Th1 responses. We further showed that the anti-CD137 mAb also had the same effects on CD3⁺CD56⁺ cells expanded from the PBMCs of patients with NSCLC. We concluded that CD137 signaling could enhance the abilities of CIK cells to kill tumor cells in vitro and in vivo via increasing the proportion of CD3⁺CD56⁺ cells and their cytotoxicity. Furthermore, CD137 signaling can elevate the capacity of CD3⁺CD56⁺ cells to induce CD4⁺ Th1 responses which may enhance their anti-tumor activity indirectly. Taken together, our studies could be considered as valuable in CIK cells-based cancer immunotherapy.     

CD4+CD25+和CD8+调节性T细胞的作用机制

调节性T细胞（Treg）主要在机体免疫系统中发挥负向调节作用,既能抑制不恰当的免疫反应,又能限定免疫应答的范围、程度及作用时间,对CD4^＋和CD8^＋效应性T淋巴细胞的增殖起抑制作用,因此在移植物抗宿主病、自身免疫病、过敏性疾病等的发病机制和临床治疗中有潜在的应用价值.本文重点介绍CD4^＋CD25^＋Treg和CD8^＋Treg的作用机制,并简述调节性T细胞研究面临的挑战与展望.     

CD8alpha- CD11b+ dendritic cells present exogenous virus-like particles to CD8+ T cells and subsequently express CD8alpha and CD205 molecules

Recombinant porcine parvovirus virus-like particles (PPV-VLPs) are particulate exogenous antigens that induce a strong, specific cytotoxic T lymphocyte (CTL) response in the absence of adjuvant. In the present report, we demonstrate in vivo that dendritic cells (DCs) present PPV-VLPs to CD8+ T cells after intracellular processing. PPV-VLPs are captured by DCs with a high efficacy, which results in the delivery of these exogenous antigens to 50% of the whole spleen DC population. In vivo, a few hours after injection, PPV-VLPs are presented exclusively to CD8+ T cells by CD8alpha- DCs, whereas 15 hours later they are presented mainly by CD8alpha+ DCs. After PPV-VLPs processing, a fraction of CD11b+ DCs undergo phenotypic changes, i.e., the up-regulation of CD8alpha and CD205 and the loss of CD4 molecules on their surface. The failure to detect mRNA coding for CD8alpha in CD11b+ DCs suggests that CD8alpha expression by these cells is not due to de novo synthesis. In recombination-activating gene knockout mice (Rag-/-), CD11b+ DCs did not express CD8alpha and PPV-VLPs presentation by CD8alpha+ DCs was severely diminished. These results indicate that both CD8alpha- and CD8alpha+ DCs play an important role in the induction of CTL responses by exogenous antigens, such as VLP.     

Microvascular thrombosis and CD40/CD40L signaling

Summary. Background: Although inflammation and thrombosis are now recognized to be interdependent processes that activate and perpetuate each other, the signaling molecules that link these two processes remain poorly understood. Objectives: The objective of this study was to assess the contribution of the CD40/CD40L signaling system to the enhanced microvascular thrombosis that accompanies two distinct experimental models of inflammation, that is, endotoxemia (lipopolysaccharide [LPS]) and dextran sodium sulfate (DSS)‐induced colitis. Methods: Thrombosis was induced in cerebral (LPS model) and cremaster muscle (DSS model) arterioles and venules of wild‐type (WT) mice and mice deficient in either CD40 (CD40^?/?) or CD40L (CD40L^?/?), using the light/dye (photoactivation) method. Results and conclusions: A comparison of thrombus formation between WT and mutant mice revealed a role for CD40 and/or CD40L in the inflammation‐enhanced thrombosis responses in both of the cerebral and muscle vasculatures. However, the relative contributions of CD40 and its ligand to thrombus formation differed between vascular beds (brain vs. muscle) and vessel types (arterioles vs. venules). The protective effect of CD40L deficiency in cerebral arterioles exposed to LPS was significantly blunted by administration of soluble CD40L. These findings implicate CD40 and its ligand in the enhanced thrombus formation that is associated with acute and chronic inflammation.     

哮喘患儿CD8+CD28+、CD8+CD28-T淋巴细胞检测及其临床意义

目的通过对哮喘患儿CD4、CD8和CD28的联合检测,探讨哮喘患儿淋巴细胞免疫功能状态及其临床意义.方法采用流式细胞术检测哮喘患儿外周血的总T细胞(CD3+)、辅助/诱导T淋巴细胞(CD4+)、抑制/细胞毒T淋巴细胞(CD8+)、细胞毒T细胞(CD8+CD28+)、抑制T细胞(CD8+CD28-).结果哮喘患儿组与对照组比较;CD3+、CD4+、CD8+CD28-细胞均低于对照组(P＜0.01,P＜0.05),CD8+CD28+细胞增高(P＜0.05),CD4+/CD8+比值、CD8+与对照组比较均无显著性差异(P＞0.05).结论哮喘患儿存在T淋巴细胞亚群免疫功能紊乱,而CD8+CD28+、CD8+CD28-T细胞失衡可能是导致机体免疫功能紊乱的主要因素.     

Differential increase of CD34, KDR/CD34, CD133/CD34 and CD117/CD34 positive cells in peripheral blood of patients with acute myocardial infarction

Objective Circulating progenitor cells (CPC) may contribute to cardiac regeneration and neovascularization after acute myocardial infarction (AMI). For potential therapeutic use, understanding the endogenous mechanisms after ischemia is inevitable. We investigated the absolute number, but also the subset composition of CD34+ CPC after AMI. Methods CD34+, KDR+/ CD34+, CD133+/CD34+ and CD117+/CD34+ CPC were analyzed by FACS in peripheral blood of 10 patients with acute MI (59±5 yrs, m/f=8/2) at day of AMI (day 0) and days 1–5. For comparison patients with stable coronary artery disease (CAD, n=12, 66±2 yrs, m/f=10/2) and young healthy volunteers (n=7, 26±2 yrs, m/f=3/4) were studied. Results CD34 and KDR/CD34, CD133/CD34, CD117/CD34 were increased day 3 and 4 after AMI. KDR+ fraction within CD34+ population remained unchanged (58.3±7.8% vs 55.3±10.6%), whereas CD133+ (64.9±3.1% vs 43.5±5.9%, P=0.006) and CD117+ fractions (71.7±5.6% vs 50.1±5.5%, P=0.02) were elevated. In CAD, all CPC and fractions were similar as AMI day 0. Healthy volunteers had more CD34+ than CAD and AMI day 0. Double positive CPC were also higher, but fractions were unchanged vs CAD with more KDR/CD34 in trend (72.8±10.6% vs 50.5±5.6%, P=0.058). After AMI both absolute numbers of CD34+ and their subset composition change, suggesting selective mobilization of CPC. Increased CPC after AMI never reach numbers of young healthy volunteers.     

GPC-3、CD147、CD10、CD138在肝细胞肝癌中的表达及临床意义

目的探究磷脂酰肌醇蛋白多糖-3(GPC-3)、白细胞分化抗原147(CD147)、白细胞分化抗原10(CD10)、多配体蛋白聚糖-1(又名CD138)在肝细胞肝癌(HCC)中的表达及临床意义。方法收集2014年1月至2018年12月该院行手术治疗并经术后病理证实的HCC患者肝癌组织标本120例及癌旁组织(距癌灶边缘2 cm)标本120例,行免疫组化检测,比较GPC-3、CD147、CD10、CD138在肝癌组织及癌旁组织中的表达,并分析其与肿瘤分化程度的关系。结果GPC-3、CD147、CD10在肝癌组织中的阳性率显著高于癌旁组织,CD138在肝癌组织中的阳性率显著低于癌旁组织,差异有统计学意义(P<0.05);高分化组GPC-3、CD147、CD10阳性率显著低于中低分化组,高分化组CD138阳性率显著高于中低分化组,差异有统计学意义(P<0.05)。结论GPC-3、CD147、CD10、CD138表达水平可能与HCC的发生发展相关,或可将其作为肿瘤标志物,进一步指导HCC的临床诊断及鉴别。