骨髓间充质干细胞静脉输注对猕猴细胞免疫功能的影响

 目的　评价猕猴间充质干细胞（MSC）静脉异体输注后对细胞免疫功能的影响。方法　分离培养MSC;不做其他处理,将异体MSC 静脉输注给受者猴,通过定期监测外周血象、混合淋巴细胞反应（MLR）、T细胞亚群来判断MSC输注后受者细胞免疫功能的变化。结果　成功培养了猕猴的MSC。异体MSC 输注后,受者无明显毒性反应、排异表现及血象变化。可以在一定时间内（2周左右）抑制受者T细胞在MLR中的增殖活性,受者猴A2、A3及A4输注MSC 的数量分别为4.0×105／kg、1.0×106／kg、2.0×106／kg,在输注后第14天时,MLR的相对反应值（RR）与输注前比较均明显降低,分别从（46.0±2.6）%、（40.9±2.3）%、（48.3±2.0）%降至（40.4±1.73）%、（33.0±2.1）%、（39.0±1.0）%（F＝10.19,P＝0.023;F＝2.593,P＝0.013;F＝28.431,P＝0.003）,输注后第30天时RR均恢复到输注前水平;统计结果显示,抑制程度（ΔRR）与输注MSC 数量呈正相关（F＝27.413,P＝0.038）。A4是输注MSC 数量最多的受者,输注后第14天开始,外周血CD+3、CD+3 CD+4、CD+3 CD+8细胞的百分比与输注前相比有所降低,在输注后第30天左右恢复至输注前水平。结论　单纯体内输注异体MSC,可以在一定时间内抑制受者T细胞的免疫活性;免疫抑制程度与输注MSC数量呈正相关。MSC 特殊的免疫学特性使其具有深远的临床应用价值。     

骨髓间充质干细胞表达外源性IL-12对胶质瘤C6细胞增殖的影响

目的: 探讨以骨髓间充质干细胞(mesenchymal stem cells,MSCs) 为基因治疗载体表达外源性IL-12对胶质瘤C6细胞增殖的影响.方法:分离培养大鼠MSCs, 腺病毒介导IL-12基因转染大鼠MSCs(AdIL-12-MSCs),RT-PCR 及Western Blotting检测AdIL-12-MSCs中IL-12基因mRNA及蛋白表达.MTT法检测AdIL-12-MSCs分泌的外源性IL-12对C6胶质瘤细胞增殖活性的影响,光镜下观察外源性IL-12对C6细胞形态的影响.结果:腺病毒介导IL-12基因成功转染MSCs形成AdIL-12-MSC,其IL-12基因在mRNA及蛋白水平均有明显表达.AdIL-12-MSC分泌的外源性IL-12显著抑制胶质瘤C6细胞的增殖(P<0.05).结论:转染IL-12的MSCs(AdIL-12-MSC)能够在mRNA及蛋白水平表达外源性IL-12基因,显著抑制胶质瘤C6细胞的增殖.     

骨髓间充质干细胞表达外源性IL-12对胶质瘤C6细胞增殖的影响

目的:探讨以骨髓间充质干细胞（mesenchymal stem cells,MSCs） 为基因治疗载体表达外源性IL12对胶质瘤C6细胞增殖的影响。方法：分离培养大鼠MSCs, 腺病毒介导IL12基因转染大鼠MSCs(AdIL12MSCs),RTPCR 及Western Blotting检测AdIL12MSCs中IL12基因mRNA及蛋白表达。MTT法检测AdIL12MSCs分泌的外源性IL12对C6胶质瘤细胞增殖活性 的影响,光镜下观察外源性IL12对C6细胞形态的影响。结果：腺病毒介导IL12基因成功转染MSCs形成AdIL12MSC,其IL12基因在mRNA及蛋白水平均有明显表达。AdIL12MSC分泌的外源性IL12显著抑制胶质瘤C6细胞的增殖（P<0.05）。结论：转染IL12的MSCs(AdIL12MSC)能够在mRNA及蛋白水平表达外源性IL12基因,显著抑制胶质瘤C6细胞的增殖。     

骨髓间充质干细胞在造血干细胞移植中的应用研究

造血干细胞移植(HSCT)后,干细胞的成活、分化、增殖及造血功能的恢复,影响治疗的效果,移植过程中难免会遇到诸多问题。如造血微环境的破坏,干细胞归巢问题及移植后的移植物抗宿主反应(GVHR)均影响移植成败。近年研究发现骨髓间充质干细胞(MSC)为造血微环境的重要组成成分,可分泌多种细胞因子,能够促进造血,加速干细胞归巢,还能参与免疫反应,降低T淋巴细胞反应。而MSC的这些特性恰好可以减少HSC中的以上问题。因此,国内外已将HSC与MSC共移植治疗恶性肿瘤应用于临床,并取得了良好的临床效果。     

骨髓间充质干细胞与肿瘤发病机制的相关性研究

间充质干细胞（ mesenchymal stem cells,MSCs）研究是近年来医学和生物学领域中最引人注目的热点之一。肿瘤相关骨髓间充质干细胞对肿瘤发病机制一直是研究的热门,间充质干细胞是存在于已分化组织中尚未分化的细胞,是中胚层发育的早期细胞,是骨髓中克隆性生长的基质细胞,具有较强的自我更新和增殖、分化潜能［1］。某些研究表明［2］,骨髓间充质干细胞发挥肿瘤抑制作用,在促进肿瘤的发生过程中起着广泛的癌症模型作用。事实上,骨髓间充质干细胞在许多上皮癌的亚型中已被证实为亲恶性,如乳腺癌、结肠癌、肺癌、皮肤癌或前列腺癌,骨髓间充质干细胞具有驱动造血系统恶性肿瘤的发生,如多发性骨髓瘤、白血病淋巴瘤的发生和发展。最近发现［3］骨髓间充质干细胞也会促进某些间质癌的进展,诸如骨肉瘤,认为部分是从骨髓间充质干细胞系的恶变而来。     

骨髓间充质干细胞多向分化潜能和微环境关系的研究

目的：深入研究骨髓间充质干细胞（mesenchymal stem cells,MSCs）多向分化的潜能与微环境的关系,从而为促进MSCs向目标组织细胞诱导分化创建新的实验方法。方法：大鼠MSCs进行分离,体外培养、扩增、鉴定。将MSCs向脂肪细胞和胰岛细胞方向诱导分化,并深入研究在不同的微环境下,其分化能力的差别,对照组诱导剂为含有角朊细胞生长因子（KGF）、胰岛素-转铁蛋白-硒（ITS）、尼克酰胺的无血清DMEM／F12培养基,实验组在对照组基础上添加胰腺条件培养液;对诱导的胰岛细胞进行观察、双硫腙染色,并进行葡萄糖刺激实验,测定细胞分泌胰岛素及C-肽功能。结果：培养的MSCs表现为非造血干细胞特性。其可向脂肪细胞,胰岛细胞等不同组织细胞分化。对照组和实验组均可分化为胰岛细胞,但实验组分化而成的胰岛细胞在数量和功能上均高于对照组。结论：MSCs具有多向分化潜能,其分化能力在特定的微环境下更强。     

骨髓间充质干细胞多向分化潜能和微环境关系的研究

目的:深入研究骨髓间充质干细胞(mesenchymal stem cells,MSCs)多向分化的潜能与微环境的关系,从而为促进MSCs向目标组织细胞诱导分化创建新的实验方法。方法:大鼠MSCs进行分离,体外培养、扩增、鉴定。将MSCs向脂肪细胞和胰岛细胞方向诱导分化,并深入研究在不同的微环境下,其分化能力的差别,对照组诱导剂为含有角朊细胞生长因子(KGF)、胰岛素-转铁蛋白-硒(ITS)、尼克酰胺的无血清DMEM/F12培养基,实验组在对照组基础上添加胰腺条件培养液;对诱导的胰岛细胞进行观察、双硫腙染色,并进行葡萄糖刺激实验,测定细胞分泌胰岛素及C-肽功能。结果:培养的MSCs表现为非造血干细胞特性。其可向脂肪细胞,胰岛细胞等不同组织细胞分化。对照组和实验组均可分化为胰岛细胞,但实验组分化而成的胰岛细胞在数量和功能上均高于对照组。结论:MSCs具有多向分化潜能,其分化能力在特定的微环境下更强。     

骨髓间充质干细胞定向诱导成骨分化的蛋白质组学分析

目的通过对人骨髓间充质干细胞（hBMSCs）定向诱导成骨细胞分化过程中不同分化阶段的比较蛋白质组学分析,寻找与干细胞分化的启动、进展及成熟有关的功能蛋白质,为研究干细胞的调控分化提供线索。方法采用贴壁培养法从人骨髓中分离获得hBMSCs,体外扩大培养,以成骨诱导培养体系诱导BMSCs定向成骨细胞分化,选取诱导的1、7、14、21d,分别提取未诱导细胞及诱导组细胞的总蛋白,采用荧光差异凝胶电泳技术分离各组总蛋白,图像分析检测差异表达的蛋白质点,经酶切后行蛋白肽质量指纹谱和数据库检索,鉴定差异蛋白表达。结果贴壁细胞于3d左右开始伸出突起,2～6d时细胞增殖较缓慢,逐渐长为梭形,7d开始细胞增殖迅速,细胞呈漩涡状生长,15d左右逐渐达到完全融合。碱性磷酸酶染色鉴定BMSCs向成骨诱导分化,BMSCs染色阴性,成骨细胞阳性。BMSCs与成骨细胞凝胶图像存在多个蛋白差异点,选取45个差异点,切胶作质谱分析。经质谱分析和数据库检索后鉴定到23个差异表达蛋白质点,大多数差异点蛋白的功能涉及细胞骨架形成、能量代谢、信号转导等过程。结论应用蛋白质组学方法,从功能蛋白质组学的层面阐述BMSCs定向诱导成骨分化相关的重要蛋白的变化,可以为更深入揭示BMSCs定向分化的分子机制提供依据。     

新方案诱导大鼠骨髓间充质干细胞诱导分化为神经元样细胞

目的探索体外诱导间充质干细胞分化为神经元样细胞后长期培养的可能性。方法自成年Wistar大鼠红骨髓分离培养骨髓间充质干细胞,通过克隆培养、成骨分化、成脂肪分化鉴定其特性,取第3代细胞重新接种,经b-FGF预诱导及β-巯基乙醇诱导后,换维持培养液维持培养。结果本实验分离培养的细胞克隆形成率64±1.4%,具有成骨及成脂肪分化能力。成神经元诱导分化0.5h后,多数细胞即开始呈现出神经元样外观,5h后绝大多数细胞表现出典型的神经元样外观,维持培养1周后,大多数细胞继续维持神经元样外观,72±3.6%的细胞MAP-2免疫细胞化学染色阳性。结论本实验中分离培养的细胞表现出间充质干细胞的特性,经诱导后,超过半数的细胞分化为神经元样细胞,在我们优化的培养体系中,分化的神经元样细胞可存活1周以上。     

体外诱导兔骨髓间充质干细胞定向分化为软骨细胞的实验研究

目的：研究兔骨髓间充质干细胞（BMMSCs）向软骨细胞分化的潜能。方法：将兔髂骨骨髓液进行原代和传代培养，以高糖DMEM无血清特定培养液诱导（含TGF-β2 10ng／ml、地塞米松7mol／L-10mol／L、维生素C50μmol／L），相差显微镜下观察细胞形态变化，免疫组织化学染色检测软骨特异性Ⅱ型胶原表达。结果：BMMSCs诱导后细胞体外扩增能力显著降低，细胞形态由成纤维样细胞梭形向多角形、多边形或类圆形转变，诱导21天后细胞形态变化最为显著，Ⅱ型胶原免疫组化染色深而均匀。结饿在适当条件下，体外培养的BMMSCs可定向诱导分化为软骨细胞。     

Role of IL-2, IL-4 and IL-6 in the growth and differentiation of tumor-specific CD4+ T helper and CD8+ T cytotoxic cells

We have earlier observed that 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU), a chemotherapeutic drug, cured 90-100% of mice bearing a syngeneic Ia- T-cell lymphoma (LSA) and furthermore, 100% of the BCNU-cured mice could reject homologous tumor rechallenge. In the present study, purified CD4+ and CD8+ T cells isolated from BCNU-cured mice were used to investigate the mechanism by which such T cells recognized and responded to the tumor-specific antigens. The responsiveness of CD4+ T cells to LSA was dependent on processing and presentation of tumor-specific antigens by syngenic Ia+ splenic antigen-presenting cells (APC). Such activated CD4+ T cells endogenously produced IL-2 but not IL-4 and only IL-2 acted as an autocrine growth factor inasmuch as anti-IL-2 receptor antibodies but not anti-IL-4 antibodies inhibited the CD4+ T cell proliferation. In contrast, the CD8+ T cells failed to produce endogenous growth factors when stimulated with LSA alone or with LSA plus APC, and therefore failed to proliferate. However, in the presence of exogenous recombinant IL-2 (rIL-2), CD8+ T cells could proliferate directly in response to LSA-stimulation, even in the absence of APC. Addition of exogenous rIL-4 alone to cultures induced CD4+ but not CD8+ T cells to proliferate. However, rIL-4 in the presence of rIL-2, could synergize and induce tumor-specific proliferation of CD8+ cells. These data suggested that for IL-4 to act as a T-cell growth factor, the presence of IL-2 was essential, either in the form of endogenously secreted IL-2 (CD4+ T cells) or exogenous IL-2 (for CD8+ T cells). In contrast to rIL-2 and rIL-4, rIL-6 failed to induce growth when used alone or in combination with rIL-2 or rIL-4. Furthermore, when tested individually, only rIL-2 but not rIL-4 or rIL-6 could support the cytotoxic differentiation of CD8+ T cells. The present study suggests that the early events in responsiveness to LSA tumor may involve activation of the IL-2-producing Th1 subpopulation of CD4+ helper cells which in turn activate IL-2 dependent CD8+ cytotoxic T cells. IL-4 if produced subsequently, may act synergistically with IL-2 to promote the growth of CD4+ and CD8+ T cells.     

与骨髓MSC共孵育的T淋巴细胞对白血病细胞的杀伤作用

目的 探讨经MSC诱导免疫耐受的T淋巴细胞对与MSC同源的肿瘤细胞的杀伤活性,以证实MSC诱导免疫耐受的同时,是否也削弱了移植物抗肿瘤的作用。方法 初治的白血病患者留取原代肿瘤细胞,液氮保存,诱导缓解后培养同一患者的骨髓MSC,取异体T淋巴细胞与MSC共孵育,比较与MSC共孵育的T淋巴细胞对MSC同源的肿瘤细胞的杀伤作用是否减弱。结果 与MSC共孵育后,T淋巴细胞对MSC同源的肿瘤细胞仍有杀伤作用,但与未共孵育者相比。杀伤活性减弱。结论 MSC在诱导免疫耐受的同时也削弱了GVI,的作用,提示在以MSC诱导免疫耐受预防GVHD的方案中,应考虑同时加强GVL作用,以防肿瘤复发。     

全反式维甲酸对人类骨髓间充质干细胞CD106、CD54表达影响的体外研究

目的探讨体外全反式维甲酸（ATRA）对人类骨髓间充质干细胞（BM—MSC）CD106和CD54表达的影响。方法用流式细胞术检测0．01、0．1、1．0、10．0μmol／LATRA处理后BM—MSC细胞表面CD106和CD54的表达,采用MTT法测量细胞生长曲线。结果0．01、0．1、1．0、10．0μmol／L的ATRA能增加BM—MSC细胞表面CD54、CD106的表达。结论ATRA对BM—MSC细胞CD54、CD106有上调的作用。     

Proanthocyanidins inhibit UV-induced immunosuppression through IL-12-dependent stimulation of CD8+ effector T cells and inactivation of CD4+ T cells

The inhibition of UVB-induced immunosuppression by dietary grape seed proanthocyanidins (GSP) has been associated with the induction of interleukin (IL)-12 in mice, and we now confirm that GSPs do not inhibit UVB-induced immunosuppression in IL-12p40 knockout (IL-12 KO) mice and that treatment of these mice with recombinant IL-12 restores the inhibitory effect. To characterize the cell population responsible for the GSP-mediated inhibition of UVB-induced immunosuppression and the role of IL-12 in this process, we used an adoptive transfer approach. Splenocytes and draining lymph nodes were harvested from mice that had been administered dietary GSPs (0.5%-1.0%, w/w), exposed to UVB, and sensitized by the application of 2,4-dinitrofluorobenzene (DNFB) onto the UVB-exposed skin. CD8(+) and CD4(+) T cells were positively selected and transferred into naive mice that were subsequently challenged by application of DNFB on the ear skin. Naive recipients that received CD8(+) T cells from GSP-treated, UVB-irradiated donors exhibited full contact hypersensitivity (CHS) response. Naive mice that received CD4(+) suppressor T cells from GSP-treated, UVB-exposed mice could mount a CHS response after sensitization and subsequent challenge with DNFB. On culture, the CD8(+) T cells from GSP-treated, UVB-exposed mice secreted higher levels (5- to 8-fold) of Th1 cytokines than CD8(+) T cells from UVB-irradiated mice not treated with GSPs. CD4(+) T cells from GSP-treated, UVB-exposed mice secreted significantly lower levels (80%-100%) of Th2 cytokines than CD4(+) T cells from UVB-exposed mice not treated with GSPs. These data suggest that GSPs inhibit UVB-induced immunosuppression by stimulating CD8(+) effector T cells and diminishing regulatory CD4(+) T cells.     

Bone marrow contains melanoma-reactive CD8+ effector T cells and, compared with peripheral blood, enriched numbers of melanoma-reactive CD8+ memory T cells

Circulating melanoma-specific T cells can be frequently detected in patients with melanoma. Effective T-cell immunity and tumor surveillance, however, requires the presence of specific T cells in tissues populated by tumor cells. The bone marrow (BM) is a compartment frequently harboring micrometastatic tumor cells. Here, we compared directly ex vivo in peripheral blood (PB) and BM frequencies and differentiation phenotypes of T cells reactive with the melanoma-associated antigen tyrosinase and with autologous melanoma cells. Using intracellular cytokine and tetramer staining, we detected tyrosinase- and melanoma-reactive CD3+CD8+ T cells in the BM in similar or enhanced frequencies as in PB. Additional characterization of the differentiation subset using CD45RA and CCR7 revealed the presence of specific effector and memory T cells in the BM in all five patients analyzed. Remarkably, the frequency of tyrosinase- and melanoma-specific memory T cells was significantly increased in BM compared with PB. Thus, the BM may be an important compartment for tumor surveillance harboring a tumor-specific memory T-cell pool in addition to effector T cells.     

CD4+CD25+调节性T细胞与CD4+T、CD8+T细胞在结直肠癌组织中的分布

 目的 分析CD4+CD25+ FOXP3+调节性T细胞（Treg）与CD4+T、CD8+T在结直肠癌（colorectal carcinoma, CRC）组织中的分布及其与临床病理特征之间的关系。方法 收集42例CRC新鲜手术标本,应用冰冻切片、免疫组织化学SP法检测肿瘤组织和癌旁组织中FOXP3+、CD4+T和CD8+T阳性细胞数。结果 CRC患者肿瘤组织中FOXP3表达水平显著升高,与癌旁组织相比差异有统计学意义（P<0.01）;中低分化组Treg细胞数明显高于高分化组（P<0.01）;淋巴结转移组Treg细胞数明显高于无淋巴结转移组（P<0.05）;癌巢内CD4+、CD8+T细胞数及CD4+/CD8+值显著低于间质（P<0.01）;Ⅲ+Ⅳ期、淋巴结转移组癌巢内CD4+/CD8+比值显著低于Ⅰ+Ⅱ期及无淋巴结转移组（P<0.05）;CRC中Treg数量与癌巢内CD4+/CD8+比值显著负相关（r=-0.605, P<0.01）。结论 CRC的发生发展可能与其癌组织局部微环境中Treg数量变化相关,肿瘤局部Treg数量的增多与T淋巴细胞亚群比例失调可能成为肿瘤免疫逃逸的机制之一。     

肺癌患者外周血白细胞介素-17+CD4+T细胞和白细胞介素-17+CD8+T细胞表达的意义

目的 检测白细胞介素(IL)-17+CD4+T(Th17)细胞和IL-17+CD8+ T(Tc17)细胞在肺癌患者外周血中的表达水平,探讨二者在肺癌免疫中的作用及临床意义.方法 采用流式细胞术(FCM)检测60例肺癌患者及40例健康对照者外周血中Th17和Tc17细胞占CD;T细胞的比例.结果 肺癌组外周血中Th17细胞[(1.795±0.623)％]和Tc17细胞[(0.865±0.357)％]比例分别高于对照组[(1.405±0.256)％、(0.640±0.204)％],(t=28.944,P＜ 0.001;t=14.051,P＜ 0.001).两组内Th17细胞与Tc17细胞的表达水平均呈正相关(肺癌组r=0.770,P＜0.05;对照组r=0.532,P＜0.05).Th7细胞和Tc17细胞表达均与临床分期有关(F值分别为4.882、3.633,均P＜0.05),但与病理类型无关(均P＞0.05).结论 肺癌患者体内Th17细胞和Tc17细胞表达升高,二者可能参与了肺癌的发生、发展;Th17与Tc17细胞的表达水平可作为评价肺癌患者免疫功能状态的新指标,能为病情监测提供参考.     

Effects of adjuvant chemotherapy on bone marrow mesenchymal stem cells of colorectal cancer patients

BACKGROUND: Chemotherapy damages the bone marrow and that is one of the most important problems in the treatment of malignancies, particularly colorectal cancer. The aim of the present study was to assess the effects of surgical adjuvant chemotherapy for CRC patients on human MSCs using an in vitro culture system. METHODS: The bone marrows of 43 CRC patients were harvested for separation and culture of MSC at pre- and post-chemotherapy. The number of colonies forming unit-fibroblast (CFU-F) was counted. The adhesive function of MSC was assayed and the growth of colony-forming unit-mixed hematopoietic cell (CFU-Mix) on the MSC layer was observed. The concentration of IL-6, SCF and FLT-T3 proteins in the MSC culture supernatant were also detected by ELISA assay. RESULTS: In the CRC patients with chemotherapy, we have demonstrated that the CFU-F exhibit significantly decreased. We also showed that the adhesive rate of bone marrow mesenchymal stem cell (BMSC) was significantly decreased. The growth of CFU-Mix on the MSC layer was inhibited. Most importantly, decreased CFU-F and the adhesive rate of BMSC were correlated significantly with decreased interleukins and stem-cell factor (IL-6, SCF and FLT-3L) expressions in the CRC patients after chemotherapy. CONCLUSION: Our results suggest that MSCs of CRC patients can be damaged by chemotherapy. Our data also indicates that the decreased expression of haematogenesis factors may play an important role in the pathogenesis. In the future, the MSC refused may have a potential clinical application in chemotherapeutically treated patients.     

Human and viral interleukin-10 in Hodgkin's disease,and its influence on CD4+ and CD8+ T lymphocytes

The Epstein-Barr virus (EBV) is closely related to Hodgkin's disease (HD), while the BCRF-I (viral [v] IL-10) gene of the EBV is highly homologous to the human interleukin-10 (h IL-10) gene. To investigate the relationship of IL-10 and HD, we performed both immunostaining and in situ hybridization (ISH) in 30 cases of HD. The presence of EBV in Hodgkin (H) and Reed-Sternberg (RS) cells was seen in 16 of the 30 cases, by ISH of the EBV EBER-I region and/or immunostaining of latent membrane protein (LMP-I). Of the 16 EBV-positive cases, 12 also showed IL-10 antigen (Ag) in H and RS cells by immunostaining, 5 of the 16 demonstrated hIL-10 RNA by ISH and 14 of the 16 showed vIL-10 RNA. But only 2 of the 14 EBV-negative cases showed IL-10 Ag, and one of them showed hIL-10 RNA, while none demonstrated vIL-10 RNA. The T cells in the HD-involved tissues were found to be mainly CD4-positive T cells, and had no association with EBV infection. However, the lymphocytes surrounding H and RS cells were more frequently CD4 cells and rarely CD8 cells in the EBV-positive cases, in contrast with the EBV-negative cases. The above results indicate that an EBV infection influenced both cytokine synthesis and the response of T cells in HD. © 1995 Wiley-Liss Inc.     

骨髓间充质干细胞表面分子CD166和CD271在胃组织中的表达

目的:探讨骨髓间充质干细胞表面分子CD166和CD271在正常胃黏膜、腺瘤及胃腺癌中的表达,初步探讨二者是否可以作为胃癌干细胞的标志物。方法:采用免疫组化染色SP法,对60例胃腺癌、10例正常胃组织标本和20例腺瘤的胃黏膜组织进行了骨髓间充质干细胞表面分子CD166和CD271的检测。结果:CD166在正常胃黏膜、不典型增生和胃癌中的表达逐渐降低,CD166在胃腺癌中的表达强度与胃癌的分化程度呈正相关（r=0.597,P<0.01）,与浸润深度有关（P<0.01）。CD271在正常胃黏膜、不典型增生中几乎不表达,在胃癌中呈低表达,CD271在胃腺癌中的表达强度与浸润深度（P<0.01）、淋巴结转移有关（P<0.01）,与患者的年龄、性别、肿瘤分化程度无关。结论:正常胃黏膜、腺瘤和腺癌的组织中存在着骨髓间充质干细胞表面分子CD166的表达,阳性细胞的位置分布没有规律性,不是胃癌肿瘤干细胞的特异性标记物,CD271在正常胃黏膜、腺瘤中几乎不表达,在胃癌中呈低表达,阳性细胞的位置分布没有规律性,不能作为胃癌肿瘤干细胞的标记物。