激发型抗CD40单克隆抗体对CD40+B细胞恶性肿瘤的生长抑制和促凋亡作用

目的　研究CD40 抗原在恶性B淋巴细胞肿瘤中的表达及其CD40 抗原激发所致的生物学效应。方法　将激发型CD40 单克隆抗体 (单抗 ) 5C11加入肿瘤细胞的体外培养体系 ,采用细胞计数、流式细胞仪分析等方法分析单抗 5C11对不同肿瘤细胞株的作用。结果　 5C11能引起CD40 表达强阳性的多发性骨髓瘤 (MM)细胞XG2发生同型聚集 ,抑制其生长并介导细胞凋亡 ;5C11可引起CD40 的恶性B淋巴瘤细胞株Daudi发生同型聚集 ,抑制其生长并使细胞发生G2 M期阻滞 ,但并不介导细胞凋亡。结论　激发型CD40 单抗通过诱导恶性B淋巴瘤细胞的凋亡或使G2 M期细胞阻滞 ,抑制肿瘤细胞的体外生长     

体外诱导人脐血树突状细胞介导T细胞抗白血病的细胞毒性效应研究

为了研究脐血淋巴细胞能否在体外培养成为特异性杀伤白血病细胞的杀伤性T细胞(CTL),联合细胞因子体外诱导脐血单个核细胞分化为树突状细胞(DC),再吞噬凋亡白血病细胞并将其抗原呈递给相同脐血的T淋巴细胞,得到杀伤性T细胞。用形态学及流式细胞术检测DC。CTL细胞的杀伤功能用乳酸脱氢酶(LDH)释放法测定。结果表明:12份脐血标本均可培养出形态典型的DC,DC的表面标志CD1a 、HLA DR 、CD86 、CD83 表达水平显著升高(P<0.05)。CTL可以杀伤未经培养的白血病细胞(效∶靶=50∶1对AML细胞的平均杀伤率为44.76±17.42%,对ALL细胞的平均杀伤率为8.50±4.25%),对相同患者缓解期的骨髓细胞杀伤率极低。结论: 在外体应用多种细胞因子刺激可诱导脐血单个核细胞分化成典型的DC;负载有白血病抗原的DC可诱导同一脐血的淋巴细胞生成白血病特异的杀伤性T细胞(CTL),所得CTL可特异性杀伤未经培养的白血病细胞而不严重伤害相同患者缓解期的骨髓细胞。     

组合性细胞因子与钙离子载体诱导急性髓系白血病细胞向树突状细胞分化中的作用

目的：探讨钙离子载体能否诱导急性髓系白血病细胞分化为树突状细胞及其抗肿瘤免疫。方法：选择2004-01／09解放军广州军区广州总医院血液科住院的初诊或复发的急性髓系白血病患者7例。分离急性髓系白血病患者的急性髓系白血病细胞，在体外给予钙离子载体100μg/L培养3-5d（钙离子载体组），或1000U／mL重组人粒细胞-巨噬细胞集落刺激因子、1000U／mL白细胞介素4和500U／mL肿瘤坏死因子α培养7-10d（组合细胞因子组）。通过细胞形态的观察及细胞免疫表型的检测鉴定树突状细胞，用同种异体混合淋巴细胞实验及细胞毒实验检测树突状细胞的功能。结果：①形态学观察和免疫表型变化：钙离子载体组及组合细胞因子组诱导急性髓系白血病细胞均可获得具有典型树突状细胞形态及免疫表型的成熟树突状细胞，但钙离子载体组诱导的树突状细胞表面CD80，CD86，CD83，CD40，CD54等分子的表达较组合细胞因子组明显增高。②混合淋巴细胞反应和胞毒性T淋巴细胞活性：钙离子载体组所诱导的急性髓系白血病细胞刺激同种异体混合淋巴细胞反应的能力及激发细胞毒性T淋巴细胞的活力比组合细胞因子组强。结论：钙离子载体能高效诱导急性髓系白血病细胞分化成树突状细胞，比组合细胞因子诱导分化的树突状细胞功能更强。     

组合性细胞因子与钙离子载体诱导急性髓系白血病细胞向树突状细胞分化中的作用

目的:探讨钙离子载体能否诱导急性髓系白血病细胞分化为树突状细胞及其抗肿瘤免疫。方法:选择2004-01/09解放军广州军区广州总医院血液科住院的初诊或复发的急性髓系白血病患者7例。分离急性髓系白血病患者的急性髓系白血病细胞,在体外给予钙离子载体100μg/L培养3～5d(钙离子载体组),或1000U/mL重组人粒细胞-巨噬细胞集落刺激因子、1000U/mL白细胞介素4和500U/mL肿瘤坏死因子α培养7～10d(组合细胞因子组)。通过细胞形态的观察及细胞免疫表型的检测鉴定树突状细胞,用同种异体混合淋巴细胞实验及细胞毒实验检测树突状细胞的功能。结果:①形态学观察和免疫表型变化:钙离子载体组及组合细胞因子组诱导急性髓系白血病细胞均可获得具有典型树突状细胞形态及免疫表型的成熟树突状细胞,但钙离子载体组诱导的树突状细胞表面CD80,CD86,CD83,CD40,CD54等分子的表达较组合细胞因子组明显增高。②混合淋巴细胞反应和胞毒性T淋巴细胞活性:钙离子载体组所诱导的急性髓系白血病细胞刺激同种异体混合淋巴细胞反应的能力及激发细胞毒性T淋巴细胞的活力比组合细胞因子组强。结论:钙离子载体能高效诱导急性髓系白血病细胞分化成树突状细胞,比组合细胞因子诱导分化的树突状细胞功能更强。     

急性髓细胞白血病细胞来源的树突状细胞的诱导及功能研究

为了研究急性髓细胞白血病(AML)细胞诱导成树突状细胞(DC)的方法及其DC的功能，分离25例AML患者骨髓或外周血单个核细胞，在含有细胞因子rhGM—CSF，rhIL-4，rhTNF—α的IMDM完全培养基中培养8—12天，进行细胞形态学、表型、遗传学及功能测定。结果表明：20／25例自诱导培养的第3天起，在倒置显微镜下可观察到部分细胞体积增大，形态由圆形变得不规则，可见驼峰样或细刺状胞浆突起；在第8—9天，该类细胞所占的比例达到峰值。至第12天，细胞总数及上述形态的细胞数量明显减少。诱导培养结束时收集细胞，应用流式细胞术检测11／20例诱导前后细胞表面标志的表达，结果表明诱导前细胞不表达CD1a、CD80及CD83，低表达CD86、CD54和HLA—DR；诱导后细胞CD1a、CD80、CD83、CD86、CD54及HLA—DR的表达明显上调。在同种异体混合淋巴细胞反应(Allo-MLR)中，该类细胞刺激同种异体淋巴细胞增殖一对^3H-TdR的摄取能力明显高于AML细胞。FISH证实诱导生成的具有DC特征细胞的AML起源。结论：体外联合应用细胞因子可将AML细胞诱导成具有DC形态、表型及功能特征的细胞(AML—DC)。     

慢性粒细胞白血病树突状细胞瘤苗对T淋巴细胞刺激作用的研究

目的　观察细胞因子联合培养诱生的白血病树突状细胞 (DC)表型和抗原提呈功能。方法　慢性粒细胞白血病细胞和K5 6 2细胞应用GM CSF IL 4 TNF α联合培养后进行细胞表型和激活淋巴细胞对白血病细胞杀伤活性的检测。结果　CML DC和K 5 6 2 DC具有DC的形态特征和超微结构 ,表达CD1a、CD80和CD86等DC相关抗原 ,并可激活淋巴细胞产生增殖反应 ,并产生针对白血病细胞的特异性细胞毒性 ,同时此种DC可不同程度地分泌IL 12并协助淋巴细胞产生IFN γ。结论　慢性粒细胞白血病细胞和K5 6 2细胞在细胞因子的诱导下 ,可分化为具有DC形态和功能的特异性抗原提呈细胞。     

钙离子载体促进K562细胞诱导分化成DC样细胞的研究

目的 观察钙离子载体(CI)诱导慢性髓系白血病细胞株K562分化成DC样细胞的作用.方法 将细胞分三组培养:第1组加入GM-CSF 1 000 U/ml和IL-4 500 U/ml;第2组加入GM-CSF 1 000 U/ml、IL-4 500 U/ml 和CI 375 ng/ml;第3组为对照,不加细胞因子,也不加CI.流式细胞仪检测各组细胞表面免疫表型的表达,MTT 比色法检测其刺激同种异体T 细胞增殖的作用.结果 细胞因子加CI 组培养48 h后即可见细胞形态呈多形性,有些细胞可见突起;96 h后CD80、CD86、CD83的表达率较对照组、单用细胞因子明显提高,明显刺激同种异体T 淋巴细胞增殖.单用细胞因子组培养96 h后细胞形态无明显变化,CD80、CD86的阳性率明显高于对照组,CD83与对照组之间差异无统计学意义,不能明显刺激同种异体T 淋巴细胞增殖.结论 CI与GM -CSF和IL-4联合可迅速将K562细胞诱导成DC样细胞;CI与细胞因子可能有协同作用.     

树突状细胞激活介导的炎性反应与主动脉夹层

目的　研究急性主动脉夹层 (AD)患者树突状细胞 (DC)的功能 ,探讨发病与炎性反应的关系。方法　分离 11例AD和 11例正常人外周血单个核细胞 (PBMC) ,在含粒细胞巨噬细胞集落刺激因子 (GM -CSF)和白细胞介素 4 (IL - 4 )的培养条件下制备DC。用流式细胞仪检测DC表面共刺激分子CD86 (B7- 2 )的表达 ;混合淋巴细胞反应 (MLR)检测DC对同种异体T淋巴细胞的刺激能力 ;ELISA法测定MLR上清液及血清中的细胞因子 ;比浊法测定循环血C -反应蛋白 (CRP)水平 ,探讨CD86表达与CRP的相关性。结果　与对照组比较 ,AD患者DC表面CD86的表达明显增高 ,对T淋巴细胞刺激的能力增强 ,MLR上清液中及血液中致炎细胞因子 (IL - 1β、IL - 6、TNF -α)升高 ,抑炎细胞因子 (IL - 10 )降低 ,血CRP水平显著升高 ,CD86的表达与血CRP水平呈正相关。结论　AD患者DC的功能显著亢进 ,由此启动的T淋巴细胞增殖和炎性细胞因子分泌可能在AD的发生发展中起重要作用。     

脐血CD34+细胞体外扩增诱导成熟树突状细胞实验研究

目的建立体外诱导和扩增人脐血树突状细胞（DC）的方法，并进行生物学鉴定。方法脐血细胞经免疫磁珠法分离纯化为CD34^＋细胞，加入细胞因子（GM-CSF和TNF-α培养约2周，光镜观察培养的DC形态学特征；通过与同种T细胞混合培养，采用MTT比色分析法测定不同浓度的DC激发同种T细胞增殖的能力。结果培养的DC胞浆突起大而长，呈树突状，具有DC的典型形态，并且具有强烈的激发同种异体T细胞增殖的能力。结论从脐血细胞分离纯化CD34^＋细胞，加入细胞因子（GM-CSF和TNF-α培养，能获得大量、较高纯度的DC。DC具有强烈的激发同种异体T细胞增殖的能力。     

人参皂苷Rg3促树突状细胞诱导作用的实验研究

目的 研究人参皂苷Rg3联合细胞因子对单核细胞来源树突状细胞(DC)的诱导及其免疫功能的影响.方法 选取8例健康志愿者分离外周血单核细胞,利用人参皂苷Rg3联合细胞因子(GM-CSF、IL-4、TNF-α)培养14 d诱导DC,光镜和电镜观察细胞形态,用流式细胞仪检测细胞免疫表型,同种异体混合淋巴细胞反应(MLR)检测其抗原呈递能力.结果 (1)单核细胞经人参皂苷Rg3联合细胞因子诱导均产生了不同比率的具有树突状细胞形态学特征的DC.这些细胞表达DC的表面分化抗原,能刺激产生MLR反应.(2)Rg3(5.0 μg/ml)联合细胞因子(GM-CSF 150 ng/ml,IL-4 50 ng/ml,TNF-α 40 ng/ml)使单核细胞-DC获得率(以CD80、CD86双阳性定义DC)由43.31%提高到59.75%,并提高了DC刺激淋巴细胞的增殖能力.结论 人参皂苷Rg3联合细胞因子可以将正常人单核细胞体外诱导成为形态、表型和功能符合DC特征的细胞,可使单核细胞诱导DC产率增加,并提高其抗原呈递功能.     

VEGF对白血病树突状细胞诱导CTL杀伤活性的影响

目的观察血管内皮生长因子(VEGF)对白血病树突状细胞(DC)激活的CTL体外杀伤活性的影响。方法K562白血病细胞经5μmol/L VEGF反义寡核苷酸作用24 h后诱导生成DC。流式细胞术检测DC特征性表型(CD40、CD86、HLA-DR和CD83)的表达,MTT法检测DC激发的细胞毒T淋巴细胞(CTL)对靶细胞的杀伤活性。ELISA法检测DC上清中IL-12的表达。结果与正常K562诱生的DC(K562-DC)相比,K562经反义寡核苷酸下调VEGF表达后培养出具有典型特征的DC(AS-K562-DC),它不仅高表达DC免疫表型,而且激活的CTL对K562细胞具有更强的杀伤效应,同时具有更强的IL-12分泌能力(P均<0.05)。结论抑制白血病细胞VEGF表达,能够促进白血病源DC的分化和成熟,激活的CTL在体外具有更强的抗白血病效应。     

Interleukin 1 production during accessory cell-dependent mitogenesis of T lymphocytes

We have studied the control and significance of IL-1 production in human leukocyte cultures during accessory cell-dependent, T lymphocyte mitogenesis using sensitive bioassays and immunolabeling techniques. In primary antigen-dependent systems like the MLR, IL-1 production was not detected in accessory cells (monocytes, dendritic cells) or T cells, suggesting that it is not an early product in these responses. However, monocytes could be induced to make IL-1 after interacting with sensitized antigen-specific T cells. Both alloreactive T cell clones or freshly prepared lymphoblasts induced IL-1 provided the monocytes carried the HLA-DR antigens to which the T cells were initially sensitized. Even in these circumstances, dendritic cells and B cells failed to make IL-1. The mechanism whereby activated T cells induce IL-1 in monocytes was explored. Supernatants from cocultures of monocytes and T cells or several recombinant cytokines induced little or no IL-1. A more potent antigen independent pathway of IL-1 induction was identified. IL-1 could be induced in third-party HLA-DR nonspecific monocytes in cocultures of alloreactive T cell clones or blasts and HLA-DR-specific dendritic cells. The induction was factor independent since dendritic cells and T blasts placed in a chamber separate from third-party monocytes by a semipermeable membrane did not induce monocyte IL-1. These results suggest that a cell contact mechanism rather than an IL-1-inducing factor leads to IL-1 production. The role of IL-1 in T cell proliferation was tested with a polyclonal anti-IL-1 antibody. The antibody failed to block the proliferation of primary T cells, or alloreactive T cell clones and blasts stimulated with HLA-specific monocytes or dendritic cells, even though IL-1 in the medium was neutralized.     

Mature T-lineage leukemia with growth factor-induced multilineage differentiation

We report an acute T-lymphoblastic leukemia with a predominantly mature CD3+ CD7+ WT31+ phenotype that was induced to differentiate into different cell lineages by various recombinant human growth factors. In the presence of IL-3 or GM-CSF, the leukemic cells gave rise to myeloid and monocytic cells including terminally differentiated, partially functional, segmented neutrophilic granulocytes as assessed by morphologic, cytochemical, immunophenotypic, and functional criteria. In the presence of IL-2, leukemic granulated lymphoid cells exhibiting MHC-unrestricted cytotoxicity and expressing a CD2+ CD3+ CD5+ CD7+ CD8+ CD33+ WT31+ Leu19+ phenotype arose. Leukemic cell cultures initiated with IL-3 yielded growth factor-independent cells with a mixed lineage phenotype and morphologic and cytochemical evidence of immature blasts. These were T lymphocyte and myeloid surface antigen (CD2,CD3,CD5,CD7,CD13,CD33,WT31) positive. Identical rearrangements of the constant region of the TCR-delta gene and of the joining regions of the TCR-beta, -gamma, and -delta genes were observed in the fresh and all cultured leukemic cells, indicating that they were derived from the same malignant clone. Consistent with the molecular genetic data, the cytogenetic analyses of the GM-CSF-, IL-3-cultured and the growth factor-independent leukemic cells showed the presence of multiple, closely related abnormal clones, all of which had an interstitial deletion of part of the long arm of chromosome 6 and a complex 1;10;12 translocation. In conclusion, these data demonstrate the involvement of a multipotent leukemic precursor cell in this predominantly mature CD2+ CD3+ CD5+ CD7+ WT31+ T-ALL. This multipotent leukemic precursor may be susceptible to various growth factors and respond with ordered differentiation and maturation.     

白血病细胞系来源的树突状细胞诱导及其抗肿瘤免疫功能研究

树突状细胞（DC）在抗肿瘤免疫反应中起关键作用，但大多数白血病病病人有DC功能缺陷，在外体扩增DC并增强其抗肿瘤免疫功能及以DC为基础的肿瘤疫苗是对白血病有效的免疫治疗方法，为了探讨由不同的髓性白血病细胞诱生DC的条件及其抗白血病反应，选用HL－60，K562和THP－1细胞与不同的细胞因子组合诱生DC，以光学和电子显微镜术观察形态特征，用流式细胞术和单克隆抗体检测细胞表型，以同种混合淋巴细胞反应观察刺激淋巴细胞增殖，用^51Cr释放法检测诱生细胞的细胞术和单克隆抗体检测细胞表型，以同种混合淋巴细胞反应观察刺激淋巴细胞增殖，用^51Cr释放法检测诱生细胞的细胞毒作用，用ELISA法测定DC培养及DC＋血单个核细胞培养的血清中IL－12及INF－γ的量，结果表明，由K562，HL－60和THP－1细胞诱生的DC具有村突状细胞的形太学特征，细胞表达DC的表面分化抗原，其中GM－CSF＋IL－4＋TNF-γ刺激HL－60－DC和THP－DC和GMCSF＋IL－4＋IL－12刺激的K562－DC中有抗原表达。3种细胞诱生的DC对混合淋巴细胞反应CTL反应有强刺激细胞因子能诱导髓性白细胞产生DC，不同细胞需要不同的细胞因子和培养条件，这些DC表达抗原呈递细胞的表型具有刺激T淋巴细胞增殖和诱导CTL反应以及分泌IL－2和促进T细胞分泌INF－γ的作用。     

TSLP-activated dendritic cells induce an inflammatory T helper type 2 cell response through OX40 ligand

We recently showed that dendritic cells (DCs) activated by thymic stromal lymphopoietin (TSLP) prime naive CD4(+) T cells to differentiate into T helper type 2 (Th2) cells that produced high amounts of tumor necrosis factor-alpha (TNF-alpha), but no interleukin (IL)-10. Here we report that TSLP induced human DCs to express OX40 ligand (OX40L) but not IL-12. TSLP-induced OX40L on DCs was required for triggering naive CD4(+) T cells to produce IL-4, -5, and -13. We further revealed the following three novel functional properties of OX40L: (a) OX40L selectively promoted TNF-alpha, but inhibited IL-10 production in developing Th2 cells; (b) OX40L lost the ability to polarize Th2 cells in the presence of IL-12; and (c) OX40L exacerbated IL-12-induced Th1 cell inflammation by promoting TNF-alpha, while inhibiting IL-10. We conclude that OX40L on TSLP-activated DCs triggers Th2 cell polarization in the absence of IL-12, and propose that OX40L can switch IL-10-producing regulatory Th cell responses into TNF-alpha-producing inflammatory Th cell responses.     

The generation of leukemic dendritic cells from acute myeloid leukemia cells is potentiated by the addition of CD40L at the terminal maturation stage

Leukemic dendritic cells (DCs) that are derived from acute myeloid leukemia (AML) cells display low-level expression of several key molecules. We investigated the optimal combination of cytokines needed to generate potent leukemic DCs from AML cells in vitro. AML cells were cultured in the presence of the following combinations of cytokines: Group A, granulocyte-macrophage colony-stimulating factor (GM-CSF) + interleukin-4 (IL-4) + tumor necrosis factor-alpha (TNF-alpha); Group B, GM-CSF + IL-4 + CD40L; and Group C, CD40L addition at the terminal maturation point of cells that were grown as for Group A. The AML cells showed clear upregulation of CD80, CD83, CD86, CD40, and HLA-DR expression under all culture conditions, without significant differences between these groups. However, the addition of CD40L (as in Group C) showed a slight upregulation in the expression of CD83 and CD86 on leukemic DCs. The leukemic DCs in Groups A and B had higher allogeneic T-cell stimulatory capacities than untreated AML cells, and the addition of CD40L (Group C) enhanced this effect. The function of the cytotoxicity-stimulating autologous T cells was also augmented by the addition of CD40L (Group C). These results suggest that AML cells may be used to generate leukemic DCs using various cytokine combinations, and that the most potent, mature leukemic DCs are generated by the addition of CD40L to terminal-stage AML cultures that are grown in the presence of conventional cytokine combinations.     

Effects of gamma-irradiation on acute myelogenous leukemia blasts: in vitro studies of proliferation, constitutive cytokine secretion, and accessory cell function during T cell activation

Generation of cellular immune responses against acute myelogenous leukemia (AML) blasts is a possible therapeutic approach in leukemia therapy. However, when using native AML blasts as stimulator cells during ex vivo generation of leukemia-reactive T cells, one has to ensure that the T cell population is not contaminated with proliferating AML blasts. Our results demonstrate that gamma-irradiation could be used to stop AML blast proliferation for all patients investigated. However, gamma-irradiation also caused a dose-dependent reduction in the constitutive AML blast secretion of the potentially T cell stimulatory cytokines IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha). At the same time, gamma-irradiation resulted in a dose-dependent decrease in anti-CD3-stimulated proliferative responses of T cell clones in the presence of AML blast accessory cells. When using 50 Gy irradiation, however, AML blast expansion was avoided, and anti-CD3 and PHA-stimulated T cell proliferation was detected in the presence of accessory AML blasts for most AML/T cell combinations investigated. When AML blasts were cultured with GM-CSF + IL-4 to develop a dendritic cell phenotype, enhanced T cell proliferation in the presence of in vitro precultured AML blasts was observed for most patients even after 50 Gy irradiation. We conclude that when using native AML blasts as accessory cells during in vitro generation of leukemia-reactive T cells, an irradiation dose of 50 Gy can be used for a majority of AML patients to avoid the risk of leukemia cell expansion during culture and with the maintenance of AML blast accessory cell function. However, when in vitro expanded cells are used in clinical trials, this antiproliferative effect should be documented with appropriate in vitro testing for every patient so that the possibility of decreased sensitivity to gamma-irradiation in exceptional patients is excluded.     

致敏的脐血源树突状细胞诱导CTL特异杀伤白血病细胞的实验研究

探讨脐血单个核细胞（MNC）诱导的树突状细胞（DC）通过负载冻融的HL-60、K562细胞抗原体外诱导产生细胞毒性T淋巴细胞（CTL）对HL-60、K562的杀伤作用。取脐血12份,分离MNC。在MNC中加入细胞因子GM-CSF（granulocyte monocyte colony-stimulating factor）、IL-3（interleukin 3）、SCF（stemcell factor）和EPO培养4周。使用CD83、CD1a、CD11C和CDw123单克隆抗体、流式细胞仪测定培养前后脐血DC抗原变化及扩增情况。DC通过负载HL-60、K-562白血病细胞抗原致敏T淋巴细胞产生CTL^3H-TdR掺入试验测定DC免疫刺激活性,MTT法观察CTL对HL-60、K562细胞的特异性杀伤活性。结果表明：新鲜脐血CD1a^＋、CD11c^＋、CD83^＋、CDw123^＋细胞数分别为0．27×10^5／ml、5．87×10^5／ml、1．94×10^5／ml、2．73×10^5／ml。加入上述细胞因子培养的脐血MNC分化为CD1a^＋、CD11C^＋、CD83^＋、CDw123^＋DC,经培养2—4周,DC数明显增多,分别达11．02×10^5／ml、28．24×10^5／ml、10．57×10^5／ml、18．7×10^5／ml,此后逐渐减少。细胞因子诱导脐血DC具有免疫刺激活性,且DC与CBMNC细胞比例为1：40时的刺激活性最佳。冻融法得到的HL-60、K562白血病细胞抗原致敏DC诱导的CTL对HL-60、K562细胞的杀伤率分别为（42．04±8．46）％和（31．25±11．07）％,与实验组比较有显著性差异（P〈0．01）。结论：加入细胞因子GM—CSF、IL-3、SCF和EPO培养2-4周的脐血MNC可分化为cD1a^＋、CD11C^＋、CD83^＋、CDw123^＋DC。冻融法得到的HL-60、K562白血病细胞抗原致敏DC,其诱导的CTL对HL-60、K562细胞具有特异的杀伤作用。脐血DC作为抗原呈递细胞在肿瘤免疫治疗上将起到重要作用。