IL-27基因转染对树突状细胞表型和功能的影响

目的 探讨转染IL-27基因体外对人外周血单个核细胞来源树突状细胞表型和功能的影响。方法 采集健康成人外周血,密度梯度离心法获得外周血单个核细胞,用GM-CSF、IL-4诱导树突状细胞（Dendritic cell, DC）,第5天后将DC分为3组：IL-27基因转染组、TNF-α组和阴性对照组。倒置显微镜观察DC形态;流式细胞术检测DC表面分子CD1a、CD80、CD83和CD86的表达情况;MTT法检测DC刺激T细胞增殖的能力;ELISA法检测细胞培养上清中IL-12和IFN-γ的含量。结果 转染IL-27基因后外周血单个核细胞来源DC呈现典型的成熟DC形态学特征。IL 27基因转染组DC表面CD1a、CD80、CD83和CD86表达水平较阴性对照组均明显上调（P<0.05）。IL-27基因转染组DC诱导T细胞增殖的能力较对照组DC明显增高（P<0.05）。IL-27基因转染组DC培养上清中IL-12和IFN-γ的含量均明显高于对照组DC（P<0.01）。结论 转染IL-27基因可以上调成熟DC的细胞表型,增强DC的免疫学活性。     

促进人胰腺癌Aspc1细胞凋亡

目的： 探讨 IL-27 基因对人胰腺癌Aspc1细胞凋亡的影响及其体内抗肿瘤作用。 方法： 重组载体PA317/IL-27转染Aspc1细胞,G418筛选稳定转染 IL-27 基因的Aspc1细胞（Aspc1/IL-27）。ELISA、细胞计数法和流式细胞术分别检测IL-27对Aspc1细胞IL-27表达、细胞增殖和MHC-Ⅰ类分子表达的影响。将Aspc1/IL-27、Aspc1/LXSN（稳定转染空质粒的Aspc1细胞）和Aspc1细胞接种于裸鼠右背部皮下,观察Aspc1细胞移植瘤的生长情况和小鼠的生存期;TUNEL法检测移植瘤细胞的凋亡,电镜观察移植瘤细胞的超微结构变化。 结果： 成功建立稳定转染PA317/IL-27载体的Aspc1/IL-27细胞株。Aspc1/IL-27细胞高表达IL-27,而Aspc1/LXSN和Aspc1细胞不表达IL-27（P<0.01）。PA317/IL-27载体转染不影响Aspc1细胞表面MHC-Ⅰ类分子的表达（P>0.05）。Aspc1/IL-27组裸鼠移植瘤生长速度明显慢于Aspc1/LXSN组及Aspc1组（P<0.05）,且生存期延长（P<0.05）。Aspc1/IL-27组移植瘤细胞凋亡率明显高于Aspc1/LXSN和Aspc1组\[（19.5±2.4）% vs（8.5±03）%、（9.1±0.8）%,P<0.01\]。 结论： IL-27 基因转染胰腺癌Aspc1细胞后通过诱导肿瘤细胞凋亡发挥抗肿瘤作用。     

IL-27基因对Eca109细胞在裸鼠体内的成瘤抑制作用及其机制

背景与目的:细胞因子为主的肿瘤生物治疗已成为肿瘤研究领域热点之一。本研究观察白细胞介素(interleukin,IL)-27基因转染人食管癌Eca109细胞株后在裸鼠体内的成瘤抑制作用及其机制。方法:以逆转录病毒为载体,采用基因转染的方法用G418梯度筛选法建立转染IL-27基因的Eca109细胞,RT-PCR检测其基因导入情况,ELISA法检测IL-27的分泌和其诱导外周血单个核细胞(peripheral blood mononuclear cells,PBMC)产生γ-干扰素(interferon,IFN)的能力,MTT法观察Eca109/IL-27细胞生长情况。将Eca109/IL-27、Eca109/LXSN和Eca109细胞接种于裸鼠皮下,观察其成瘤性、移植瘤的生长情况并计算抑瘤率。流式细胞技术检测移植瘤组织肿瘤浸润淋巴细胞(tumor infiltrating lymphocyte,TIL)中CD16、FasL的表达和肿瘤细胞上Fas的表达。结果:RT-PCR示Eca109/IL-27细胞中有IL-27p28和IL-27EBI3亚基基因表达,Eca109/LXSN和Eca109细胞中未见表达(P<0.01),从而成功建立稳定转染的Eca109/IL-27细胞株,ELISA检测Eca109/IL-27中IL-27的分泌量高于Eca109/LXSN和Eca109细胞(P<0.01)。IL-27基因转染不影响人食管癌细胞株的体外生长(P>0.05),Eca109/IL-27诱导PBMC产生IFN-γ含量高于Eca109/LXSN和Eca109[(56.28±1.61)pg/mL vs.(12.70±0.82)pg/mL]和(11.06±0.64)pg/mL,P<0.01),Eca109/IL-27移植瘤体积较Eca109和Eca109/LXSN减小,瘤重减轻,有抑瘤作用(P<0.05);Eca109/IL-27细胞接种的肿瘤组织TIL中CD16阳性率升高,FasL的表达增高(P<0.05),肿瘤细胞表面Fas表达增加(P<0.05)。结论:IL-27基因修饰Eca109细胞在裸鼠体内产生了抑制肿瘤生长的作用,其机制可能是通过活化自然杀伤细胞,以Fas/FasL的途径产生的。     

IL-27通过上调MIG和IP-10的表达抑制肿瘤血管形成

目的: 研究IL-27对肿瘤血管生成的抑制作用及其机制.方法:IL-27基因稳定转染的人食管癌细胞(Eca109/IL-27)接种于裸鼠,建立荷瘤裸鼠模型,观察肿瘤生长情况和裸鼠生存期.用ELISA法检测脾细胞IFN-γ的分泌水平;免疫组化法检测瘤组织中VEGF和CD34的表达,并通过CD34的水平计算微血管密度;用RT-PCR法检测肿瘤组织趋化因子IP-10、MIG mRNA的表达水平.结果:接种Eca109/IL-27细胞荷瘤小鼠的生存期较接种野生型Eca109细胞(未转染质粒)和Eca109/LXSN细胞(空载体质粒转染)小鼠的生存期明显延长(P<0.05).接种Eca109/IL-27细胞的裸鼠瘤组织中VEGF和CD34的表达水平显著性低于接种Eca109细胞和Eca109/LXSN细胞,微血管密度显著降低(均P<0.01).Eca109/IL-27组小鼠脾细胞产生较高水平的IFN-γ(P<0.05),趋化因子IP-10和MIG mRNA的表达水平也显著性高于接种Eca109细胞组和Eca109/LXSN细胞组(P<0.05).结论:IL-27在裸鼠体内通过上调IP-10和MIG表达抑制肿瘤血管生成,从而发挥抗肿瘤作用.     

白细胞介素-18基因转染的肺癌细胞与树突状细胞融合体的抗肿瘤作用

目的研究白细胞介素-18(IL-18)基因转染的肺癌细胞与树突状细胞(DC)融合体的抗肿瘤作用。方法(1)从人外周血单核细胞诱导培养DC,与IL-18基因转染的NCI-H460肺癌细胞融合,经免疫磁珠筛选。(2)设转染组(GT组)、空载体转染组(PT组)、未转染组(NT组)和对照组(BC组),分别以IL-18转染的融合细胞、pcDNA3.1~ 转染的融合细胞、未转染的融合细胞活化的T细胞为效应细胞,BC组不含效应细胞,用乳酸脱氢酶(LDH)法测定效应细胞对NCI-H460细胞的杀伤作用。(3)荷瘤裸鼠皮下注射上述3种效应细胞,以BC组为空白对照,比较4组裸鼠肿瘤体积和重量。结果3组效应细胞在体外对NCI-H460细胞的杀伤率分别为53.1%,30.1%和31.5%;3组裸鼠肿瘤体积及肿瘤重量明显低于BC组,以GT组最低。结论IL-18基因转染的融合细胞可有效诱导抗肿瘤免疫。     

肺癌细胞致敏树突状细胞疫苗的体内外抗肿瘤作用

目的:研究以NCI-H460肺癌细胞致敏的树突状细胞(Dendritic cells,DCs)疫苗的抗肿瘤作用。方法:将IL-18基因转染的NCI-H460细胞及未转染NCI-H460细胞与DC融合作为转染融合DC组及融合DC组疫苗,以NCI-H460细胞RNA冲击的DC为冲击DC组疫苗,以未冲击的DC为DC组疫苗。以MTT法检测4组DC疫苗刺激T细胞增殖的作用,用ELISA法测定DC疫苗上清液中IL-12的含量,用LDH法测定DC疫苗对NCI-H460细胞的杀伤作用。裸鼠皮下接种NCI-H460细胞及DC疫苗,观察成瘤时间及裸鼠存活情况;荷瘤裸鼠瘤内注射DC疫苗,比较肿瘤体积。结果:4组DC疫苗均能刺激T细胞增殖,刺激作用强度为转染融合DC组>融合DC组>冲击DC组>DC组;4组均能分泌IL-12,转染融合DC组IL-12的分泌量高于融合DC组,冲击DC组高于DC组;转染融合、融合、冲击DC和DC组疫苗对NCI-H460细胞的杀伤率分别为79.73%、50.68%、35.81%及4.05%。转染融合组裸鼠移植瘤成瘤时间[(12.82±2.85)d]长于冲击DC组[(8.52±1.97)d](P<0.05)和DC组[(8.33±1.63)d](P<0.01);移植瘤内注射疫苗后的肿瘤体积比较,转染融合组<融合组<冲击DC组相似文献   

黏蛋白1基因转染DC对乳腺癌细胞MCF-7裸鼠移植瘤的免疫抑制作用

目的:探讨黏蛋白1 (mucin 1,MUC1基因转染DC对人乳腺癌MCF-7细胞裸鼠移植瘤的抑制作用.方法:体外诱导培养健康成人DC,应用脂质体转染法将pcDNA3.1-MUC1转染DC,ELISA法检测转染后DC分泌细胞因子IL-12和YNF-α的能力,LDH释放法检测基因转染后DC诱导特异性CTL对乳腺癌MCF-7细胞的杀伤活性.应用MU C1基因转染DC、空质粒转染DC、及生理盐水皮下注射治疗人乳腺癌MCF-7细胞裸鼠移植瘤,观测其对肿瘤生长的抑制作用.结果:转染pcDNA3.1-MUC1的DC分泌IL-12、TNF-α的能力较转染空质粒DC明显增强[IL-12:(202.52±29.61)vs(10.83±1.02)pg/ml;TNF-α:(349.07±79.42)vs(9.26±1.52)pg/ml,均P＜0.01];转染pcDNA3.1-MUC1的DC诱导产生特异性CTL,对人乳腺癌MCF-7细胞具有更明显的杀伤活性,效靶比为10∶1、5∶1和2.5∶1时的杀伤率分别达到56.2％、38.9％和25.8％,显著高于对照组CTL(均P＜0.01).MUC1基因转染DC对乳腺癌MCF-7裸鼠移植瘤生长抑制作用明显强于空质粒转染DC组(P＜0.05).结论:MUC1基因转染DC可以诱导特异性CTL,对乳腺癌MCF-7细胞具有更强的抗肿瘤免疫效应.     

IL-27促进人胰腺癌Aspc1细胞凋亡

目的:探讨IL-27基因对人胰腺癌Aspc1细胞凋亡的影响及其体内抗肿瘤作用.方法:重组载体PA317/IL-27转染Aspc1细胞,G418筛选稳定转染IL-27基因的Aspc1细胞(Aspc1/IL-27).ELISA、细胞计数法和流式细胞术分别检测IL-27对Aspc1细胞IL-27表达、细胞增殖和MHC-Ⅰ类分子表达的影响.将Aspc1/IL-27、Aspc1/LXSN(稳定转染空质粒的Aspc1细胞)和Aspc1细胞接种于裸鼠右背部皮下,观察Aspc1细胞移植瘤的生长情况和小鼠的生存期;TUNEL法检测移植瘤细胞的凋亡,电镜观察移植瘤细胞的超微结构变化.结果:成功建立稳定转染PA317/IL-27载体的Aspc1/IL-27细胞株.Aspc1/IL-27细胞高表达IL-27,而Aspc1/LXSN和Aspc1细胞不表达IL-27(P＜0.01).PA317/IL-27载体转染不影响Aspc1细胞表面MHC-Ⅰ类分子的表达(P＞0.05).Aspc1/IL-27组裸鼠移植瘤生长速度明显慢于Aspc1/LXSN组及Aspc1组(P＜0.05),且生存期延长(P＜0.05).Aspc1/IL-27组移植瘤细胞凋亡率明显高于Aspc1/LXSN和Aspc1组[(19.5±2.4)%vs(8.5±0.3)%、(9.1±0.8)%,P＜0.01].结论:IL-27基因转染胰腺癌Aspc1细胞后通过诱导肿瘤细胞凋亡发挥抗肿瘤作用.     

K-ras 抗原致敏的DC诱导CTL 对胰腺癌体内杀伤活性的研究*

目的:研究K-ras多肽的致敏树突状细胞（DC）活化的特异性细胞毒性T 淋巴细胞（CTL）对胰腺癌的体内外杀伤作用。方法:联合应用粒细胞- 巨噬细胞集落刺激因子和白细胞介素-4 诱导培养外周血DC。表达K-ras突变体的胰腺癌细胞株全瘤、单纯K-ras突变体多肽和K-ras突变体表位肽阳离子纳米颗粒分别致敏DC。致敏DC刺激T 淋巴细胞得到肿瘤抗原特异的细胞毒性T 淋巴细胞（CTL）。 Patu 8988、SW1990细胞系制备荷瘤裸鼠模型评价CTL 体内抗肿瘤活性。结果:负载全瘤抗原的DC其诱导产生的CTL 对胰腺癌有较好的抑制,负载单纯K-ras（12-Val ）突变体多肽、K-ras（12-Val ）突变体表位肽阳离子纳米颗粒的DC其诱导产生的CTL 对表达K-ras（12-Val ）突变体阳性（Patu 8988）的胰腺癌有较特异的抑制作用,而对K-ras（12-Val ）突变体阴性（SW1990）的胰腺癌的抑制作用与对照组比较无显著性差异。结论:负载肿瘤抗原的DC诱导的CTL 可显著提高对荷瘤裸鼠的生存时间,抑制肿瘤的生长速度,并显示其可增加抗肿瘤特异性。      

Immunotherapy of spontaneous metastatic lung cancer with tumor antigen-pulsed,interleukin-12 gene-modified dendritic cells

Interleukin-12 (IL-12), with the ability of inducing production of interferon-gamma and enhancing of NK activity and Th1 response, has potent antitumor role and has been used in treatment of tumors[1-7]. Dendritic cells (DC) are the uniquely potent APCs involved in the initiation of immune responses. As adjuvants for Ag delivery, DC pick up Ags in the periphery and carry them to T cells area in lymphoid organs to prime the immune responses. With the development of the methods for propaga…     

An efficient method to prepare T cell receptor gene-transduced cytotoxic T lymphocytes type 1 applicable to tumor gene cell-therapy

Genes encoding 2C T cell receptor (TCR) α, β chains from H-2^b-re-stricted L^d-specific CD8⁺ cells were successfully transduced into polyclonally activated CD8⁺ cells by retroviral modification to generate antigen-specific cytotoxic T lymphocytes (CTL). Antigen-nonspecific CD8⁺ T cells polyclonally expanded in the presence of interleukin (IL)-2, Th1 cytokines (interferon (IFN)-γ and IL-12) and anti-IL-4 monoclonal antibody showed neither cytokine production nor cytotoxicity in response to L^d-expressing P815 tumor cells. However, 2C-TCR gene-modified CD8⁺ T cells exhibited both IFN-γ production and cytotoxicity in response to P815 tumor cells. The antitumor activity of TCR gene-modified Tc1 cells was also demonstrated in vivo by Winn's assay. Thus, we have developed an efficient method to induce TCR gene-modified antigen-specific Tc1 cells that exhibit antitumor activity both in vitro and in vivo . (Cancer Sci 2003; 94: 389–393)     

体外研究CpG基序对人食管癌疫苗的佐剂效应

目的:探讨CpG基序在人食管癌Eca-109细胞疫苗研究中的佐剂效应.方法:以Eca-109细胞膜表面小肽刺激DC作为食管癌疫苗,HL-60细胞膜表面小肽刺激DC作为对照疫苗.以CpG基序作为佐剂,以CBPw作为对照佐剂,测定各组的T细胞增殖试验和CTL活性.结果:佐剂组的T细胞活性明显高于其余各组(P＜0.01);人食管癌疫苗组的T细胞活性明显高于其余各组(P＜0.01);与Eca-109细胞匹配的HLA也影响了T细胞活性的发挥.结论:CpG基序是人食管癌疫苗的有效佐剂,HLA对T细胞功能有影响.     

Fusion hybrid of dendritic cells and engineered tumor cells expressing interleukin-12 induces type 1 immune responses against tumor

AIMS AND BACKGROUND: Dendritic cell (DC)-tumor fusion hybrid vaccinees that facilitate antigen presentation represent a novel powerful strategy in cancer immunotherapy. Preclinical studies have demonstrated that IL-12 promotes specific antitumor immunity mediated by T cells in several types of tumors. In the present study, we investigated the antitumor immunity derived from vaccination of fusion hybrids between DCs and engineered J558/IL-12 myeloma cells secreting Th1 cytokine IL-12. METHODS: The expression vector pcDNA-IL-12 was generated and transfected into J558 myeloma cells and then bone marrow-derived DCs were fused with engineered J558/IL-12 cells. The antitumor immunity derived from vaccination of the fusion hybrid DC/J558/IL-12 was evaluated in vitro and in vivo. RESULTS: DC/J558/IL-12 cells secreted recombinant IL-12 (1.6 ng/mL), and inoculation of BALB/c mice with DC/J558/IL-12 hybrid induced a Th1 dominant immune response and resulted in tumor regression. Immunization of mice with engineered DC/J558/IL-12 hybrid elicited stronger J558 tumor-specific cytotoxic T lymphocyte (CTL) responses in vitro as well as more potent protective immunity against J558 tumor challenge in vivo than immunization with the mixture of DCs and J558/IL-12, J558/IL-12 and J558, respectively. Furthermore, the anti-tumor immunity mediated by DC/J558/IL-12 tumor cell vaccination in vivo appeared to be dependent on CD8+ CTL. CONCLUSIONS: These results demonstrate that the engineered fusion hybrid vaccines that combine Th1 cytokine gene-modified tumor cells with DCs may be an attractive strategy for cancer immunotherapy.     

Route of administration influences the antitumor effects of bone marrow-derived dendritic cells engineered to produce interleukin-12 in a metastatic mouse prostate cancer model

Gene-modified dendritic cells (DC) provide unique therapeutic strategies for prostate cancer; however, the comparative evaluation of specific delivery options using appropriate preclinical models has not been described. In this study, bone marrow-derived DC were genetically engineered to express high levels of interleukin-12 (IL-12) with or without the costimulatory molecule B7-1, by ex vivo infection with recombinant adenoviral vectors. We used an orthotopic metastatic mouse prostate cancer preclinical model (178-2 BMA) to compare two therapeutic protocols for DC delivery, in situ and subcutaneous. DC were generated from bone marrow of syngeneic 129/Sv mice by culturing in the presence of GM-CSF and IL-4. In vitro DC/IL-12 or DC/IL-12/B7 produced high levels of biologically active IL-12. In situ delivery of DC/IL-12 or DC/IL-12/B7 induced a significant suppression of primary tumor growth compared to DC/beta gal controls (P=.0328 and P=.0019, respectively), as well as reduced numbers of spontaneous lung metastatic nodules (P=.1404 and P=.0335, respectively). In survival experiments, in situ DC/IL-12 injection demonstrated a small but statistically significant advantage (P=.0041). Subcutaneous, tumor lysate pulsed DC/IL-12 significantly decreased tumor size (P=.0152) and increased survival (P=0.0433) compared to HBSS controls but the decrease in the number of spontaneous lung metastases did not achieve statistical significance. Both in situ and subcutaneous treatments enhanced cytolytic activities of natural killer (NK) cells and cytotoxic T lymphocytes (CTL). In this preclinical model, gene-modified DC-based intratumoral immunotherapy was shown to be an effective therapeutic strategy for locally advanced prostate cancer based on tumor growth suppression, inhibition of metastasis and survival improvement.     

Enhanced antitumor immune responses of IL-2 gene-modified tumor vaccine by combination with IL-1 and low dose cyclophosphamide.

To enhance the antitumor immunity induced by IL-2 gene-modified tumor vaccine, we proposed a combined protocol to treat tumor-bearing mice using IL-2 gene-modified tumor vaccine in combination with IL-1 and low-dose Cyclophosphamide(Cy). After treatment with IL-2 gene-modified B16 melanoma cell vaccine alone, the pulmonary metastases of tumor-bearing mice were reduced and their survival time was prolonged. The anti-metastases effect was improved when the vaccine was used in combination with IL-1 or low-dose Cy. The best therapeutic effect was achieved when the IL-2 gene-modified vaccine was combined with IL-1 and low-dose Cy. The cytotoxicity of the splenic CTL, NK, and the levels of IL-2, TNF secreted by splenocytes increased after tumor-bearing mice were treated with the IL-2 gene-modified tumor vaccine. The above antitumor immune functions were augmented more significantly when IL-1, low-dose Cy were used in combination with IL-2 genemodified tumor vaccine. These results demonstrated that the IL-2 gene modified vaccine could exert more potent anti-metastases effects when it is combined with IL-1 or/and low-dose Cy by activating the specific and non-specific antitumor immune responses more effectively.     

DC 荷载α－GalCer 联合肿瘤特异性 CTL 对小鼠 Heps 肝癌移植瘤生长的影响

目的：探讨树突状细胞（DC）荷载α－半乳糖神经酰胺（α－GalCer）联合肿瘤特异性细胞毒 T 淋巴细胞（CTL）对小鼠 Heps 肝癌移植瘤生长的抑制作用。方法：诱导扩增小鼠骨髓来源的 DC 细胞和 T 淋巴细胞,培养成为具有肿瘤特异性的 CTL,DC 细胞体外荷载α－GalCer。建立 Heps 肝癌移植瘤模型,将36只模型鼠随机分为4组（n ＝9）,分别尾静脉给予生理盐水（对照组）、CTL（CTL 组）、DC 荷载α－GalCer（DC 荷载α－GalCer 组）、DC 细胞荷载α－GalCer ＋CTL（联合治疗组）输注。每隔两天测量移植瘤体积,观察体积变化。于治疗后第14d,处死小鼠,取眼球血及瘤体组织。流式细胞术（FCM）检测外周血 CD4＋、CD8＋ T 细胞比例。免疫组织化学染色观察肿瘤组织中 Bcl －2／Bax 凋亡蛋白的表达。结果：与对照组相比,各治疗组均可抑制肿瘤的生长,差异具有统计学意义（P ＜0．01）;联合治疗组较 DC 荷载α－GalCer 组及 CTL 组肿瘤体积明显减小（P ＜0．05）。联合治疗组小鼠外周血 CD4＋、CD8＋ T 细胞数量较另外三组显著升高（P ＜0．05）;对照组、CTL组、DC 荷载α－GalCer 组小鼠外周血中 CD4＋、CD8＋ T 细胞含量无明显差异（P ＞0．05）。与对照组相比,各治疗组移植瘤内 Bax 阳性细胞数量明显增加（P ＜0．05）,Bcl －2阳性细胞数量明显减少（P ＜0．05）;与 CTL组和α－GalCer 组相比,联合治疗组移植瘤内 Bax 阳性细胞明显增加（P ＜0．05）,Bcl －2阳性细胞明显下降（P ＜0．05）。结论：DC 荷载α－GalCer 与肿瘤特异性 CTL 联合应用能够对小鼠 Heps 肝癌移植瘤具有协同杀伤作用。     

膀胱肿瘤抗原致敏的树突状细胞诱导T淋巴细胞抗肿瘤效应的研究

目的：研究经膀胱肿瘤抗原致敏后的树突状细胞（Dc）对T淋巴细胞的激活、增殖作用及对T24膀胱肿瘤细胞的抑癌效应。方法：分离健康供血者外周血单个核细胞及T淋巴细胞，联合应用粒／巨噬细胞集落刺激因子（GM—CSF）及白介素-4（IL-4）从单个核细胞中培养出Dc，以人膀胱癌细胞系T24肿瘤细胞裂解物刺激Dc，检测经膀胱肿瘤抗原致敏后的DC对T淋巴细胞的细胞增殖动力学影响并用M1rr显色法测定致敏Dc诱导的T淋巴细胞对T24膀胱肿瘤细胞体外的抗肿瘤效应。结果：膀胱癌细胞裂解物致敏的Dc可诱导T淋巴细胞强烈的增殖反应，与对照组比较具有显著性差异（P〈0．01）；增殖后的T淋巴细胞对T24膀胱肿瘤细胞有明显的细胞毒作用。结论：经膀胱肿瘤抗原致敏的Dc能诱导产生显著的T淋巴细胞增殖，在体外有明显的抑癌效应。     

AK细胞及环磷酰胺治疗肝癌的实验研究

为研究１ 种新的过继免疫化疗治疗肝癌的方法,采用肝癌细胞株Ｈ２２ 接种于近交系Ｂａｌｂ／ｃ 小鼠皮下,制成肿瘤模型。使用ＩＬ２ 、肿瘤活化的杀伤细胞（ＡＫ细胞）及环磷酰胺（Ｃｙ） 进行治疗,检测小鼠脾淋巴细胞ＮＫ、ＬＡＫ及ＣＴＬ 活性,用流式细胞仪检测Ｌ３Ｔ４ 亚群及Ｌｙｔ２ 亚群含量。结果表明在过继免疫化疗组小鼠ＬＡＫ 及ＣＴＬ活性明显高于其它治疗组（Ｐ＜ ０．０１）,荷瘤小鼠肿瘤结节生长较ＩＬ２ 组及Ｃｙ 组明显缓慢（Ｐ＜ ０．０１）,生存期也明显高于其它各治疗组（Ｐ＜０ ．０１）。该研究表明过继免疫化疗有较强的抗肿瘤作用。