肿瘤细胞裂解物疫苗与其修饰的树突状细胞联合抗A20鼠淋巴瘤的作用

将A20淋巴瘤细胞,反复冻融,获得肿瘤细胞裂解物的抗原肽,以来源于结核分枝杆菌(Mycobacterium tuberculosis)热休克蛋白70(HSP70)第407-426(mHSP70407~426,M)的两段串联重复序列M2小肽为佐剂,通过双功能偶联试剂戊二醛偶联制备肿瘤细胞疫苗A20-M2,偶联产物在体外修饰未成熟的DC,通过检测负载肿瘤细胞抗原的DC细胞分泌的细胞因子以及抗原来确定被修饰DC细胞的成熟度,获得成熟DC即获得DC疫苗。用A20-M2与DC两种疫苗联合给药治疗小鼠,实验结果显示,激发的免疫应答对于A20肿瘤攻击起到有效的保护作用,与PBS阴性对照组比较,平均肿瘤重显著降低(P<0.01),通过ELISA法,从小鼠血清中检测到高滴度抗细胞裂解物类抗体,淋巴细胞增殖试验显示疫苗联合给药后能够有效的刺激脾淋巴细胞的增殖反应。A20-M2能够有效的刺激DC细胞成熟,A20-M2与成熟DC细胞联合给药能够有效的抑制小鼠A20淋巴瘤的生长。     

胡桃醌对小鼠黑色素瘤细胞B16F10体内迁移的影响

目的:研究胡桃醌对小鼠黑色素瘤细胞B16F10体内迁移的影响.方法:采用小鼠B16/F10黑色素瘤人工肺转移模型研究胡桃醌对肿瘤细胞血道转移的作用.结果:与溶剂对照组相比,4.5、3、1.5和0.75 mg/kg胡桃醌组显著减少小鼠黑色素瘤B16F10血道转移(P＜0.05),其抑制率分别为27.30％、55.35％、31.52％和25.34％;3 mg/kg胡桃醌与阳性对照组相比,抑瘤率无统计学差异(P＞0.05).结论:胡桃醌可抑制小鼠黑色素瘤B16F10血道转移.     

跨膜型超抗原金黄色葡萄球菌肠毒素A融合蛋白的抗肿瘤作用

目的　为扩大超抗原金黄色葡萄球菌肠毒素A(SEA)的抗瘤谱 ,制备跨膜型SEA融合蛋白 ,研究该蛋白制备的肿瘤疫苗的抗肿瘤作用。方法　在荷B16黑色素瘤的C5 7BL/ 6小鼠上 ,观察跨膜型SEA融合蛋白制备的肿瘤疫苗对荷瘤小鼠的免疫治疗作用和免疫保护作用 ,并通过乳酸脱氢酶 (LDH)释放法检测治疗组和免疫组小鼠脾细胞的天然杀伤细胞(NK)和细胞毒性T细胞 (CTL)活性。结果　融合蛋白制备的肿瘤疫苗能够显著抑制荷瘤小鼠肿瘤的生长 ,并延长其生存期 ,其脾细胞的NK和CTL活性显著增强。同时 ,该肿瘤疫苗对同种肿瘤细胞攻击可产生较强的免疫保护作用。结论　跨膜型SEA融合蛋白制备的肿瘤疫苗具有显著的抗肿瘤作用 ,可有效激发荷瘤小鼠机体的特异性和非特异性抗肿瘤免疫应答 ,增强CTL和NK活性。     

以链球菌制剂OK432为佐剂的内皮细胞疫苗体内抗小鼠肝癌转移的作用（英文）

目的评估OK432作为佐剂制备的内皮细胞疫苗体内抗肿瘤转移的作用。方法以OK432为佐剂,体外混合人脐静脉内皮细胞(HUVEC),制备HUVEC-OK432疫苗。雄性健康BALB/c小鼠尾静脉注射肝癌细胞5×105建立肝癌肺转移模型,皮下注射HUVEC-OK432疫苗,分别在预防性和治疗性免疫中评价HUVEC-OK432疫苗抗肿瘤转移活性;皮内注射5×104肝癌细胞建立皮内肿瘤血管模型,皮下注射HUVEC-OK432疫苗,评价HUVEC-OK432疫苗抑制肿瘤新生血管的活性;采用ELISA的方法测定小鼠免疫血清中HUVEC抗体水平;采用细胞毒T淋巴细胞(CTL)实验考察HUVEC-OK432疫苗诱导的细胞免疫应答水平。结果肺转移模型结果显示,在预防性和治疗性免疫中,HUVEC-OK432免疫均能有效降低小鼠肺上的肿瘤转移灶数目(P<0.01);皮内肿瘤血管模型的结果显示,HUVEC-OK432免疫能显著降低肿瘤新生血管的数目(116.5±20.6 vs 45.0±8.9,P<0.01);ELISA测定抗体的结果显示,HUVEC-OK432初次免疫后1周小鼠即产生了高滴度的特异性HUVEC抗体,随免疫次数的增加抗体水平不断升高,且该抗体在体外可以显著抑制HUVEC细胞的增殖;CTL实验的结果表明,HUVEC-OK432免疫组淋巴细胞体外有明显的特异性杀伤HUVEC的作用。结论 HUVEC-OK432疫苗免疫可以有效诱导小鼠产生靶向内皮细胞的免疫应答,从而有效抑制小鼠肝癌细胞转移。     

基于M2与OK-432的肿瘤细胞裂解物致敏的树突状细胞疫苗抗小鼠Lewis肺癌作用研究

目的：建立增强肺癌细胞裂解物（L）致敏的树突状细胞（D）疫苗（L-D）免疫临床治疗肺癌效果的方法。方法：以来源于热休克蛋白70第407~426的两段重复序列（M）和OK-432（O）为佐剂刺激Lewis肺癌细胞裂解物,制备了树突状细胞疫苗LMO-D。结果：与L-D相比, LMO-D显著增加CD11c、CD40、CD80、CD86、MHC-Ⅰ和Ⅱ等细胞表面抗原的表达;LMO-D免疫荷瘤小鼠后,显著增强Th1类细胞因子肿瘤坏死因子α和干扰素γ,而不增强Th2类细胞因子白介素-5的表达;T淋巴细胞增殖诱导显著和淋巴细胞毒反应;此外LMO-D显著降低荷瘤小鼠瘤重与体积,延长了荷瘤小鼠的生存期。结论：LMO-D可通过诱导显著的T细胞免疫反应有效抑制肿瘤生长。     

OK432优化的内皮细胞疫苗抗小鼠乳腺癌作用研究

目的探讨OK432优化的人脐静脉内皮细胞(HUVECs)疫苗对小鼠EAC乳腺癌的生长抑制作用。方法体外培养HUVECs,与佐剂OK432混合,制备HUVECs-OK432疫苗,以小鼠EAC乳腺癌皮下移植瘤模型考查HUVECsOK432疫苗的抗肿瘤效应,并通过ELISA、脾细胞增殖及细胞毒性T淋巴细胞(CTL)杀伤实验检测疫苗免疫后体液及细胞免疫应答水平。结果在预防性免疫中,HUVECsOK432疫苗可以明显抑制EAC乳腺癌生长;HUVECs-OK432疫苗诱导小鼠产生了高滴度的特异性HUVEC抗体;HUVECs-OK432疫苗能有效刺激免疫小鼠脾淋巴细胞的增殖;HUVECs-OK432组小鼠脾细胞诱导产生了明显的靶向HUVEC细胞的CTL杀伤作用。结论 HUVECs-OK432疫苗可以有效诱导机体产生靶向HUVEC的特异性体液及细胞免疫应答,从而有效抑制了小鼠EAC乳腺癌的生长。     

CpG ODN联合肿瘤抗原致敏的树突状细胞疫苗抑制和预防小鼠黑色素瘤的研究

探讨非甲基化的胞嘧啶鸟嘌呤二核苷酸(CpG)的脱氧寡核苷酸(oligodeoxynucleotide, ODN)联合肿瘤抗原致敏树突状细胞(DC)治疗和预防黑色素瘤的作用。首先从小鼠骨髓中分离得到骨髓来源的树突状细胞(BMDC),并将小鼠黑色素瘤B16细胞来源的全抗原与DC共孵育,采用全硫代修饰的CpG ODN作DC免疫刺激剂,制备DC疫苗。通过测定T淋巴细胞增殖和细胞毒性T淋巴细胞(CTL)对靶细胞B16的杀伤作用来评价该疫苗的体外免疫活性。将疫苗经小鼠腹腔注射,观察其治疗和预防小鼠黑色素瘤的效果。所有动物实验均在中国科学院上海药物研究所实验动物管理委员会(IACUC)的指导和标准下进行。结果显示, CpG ODN和肿瘤抗原联用致敏的DC疫苗能够促进T淋巴细胞增殖,并提高活化的T淋巴细胞对靶细胞B16的杀伤活性。体内实验表明,无论是治疗实验还是预防实验, DC疫苗组的平均瘤重和瘤体积均低于PBS对照组。实验结果证明基于CpG ODN和黑色素瘤肿瘤抗原制备的DC疫苗对肿瘤具有较好的抑制作用,为恶性黑色素瘤治疗提供了一个潜在的方案。     

蜂王浆冻干粉对B16-BL6黑色素瘤生长的影响

目的观察蜂王浆冻干粉(LRJ)对B16-BL6黑色素瘤生长的影响。方法体外应用MTT法观察LRJ对B16-BL6黑色素瘤生长影响。体内建立B16-BL6实体瘤模型,观察LRJ对肿瘤生长的影响,并用常规病理检测(HE染色)及原位细胞凋亡检测法(TUNEL)观察瘤组织病理变化及细胞凋亡情况。结果体外实验观察到LRJ甲醇、乙醇及乙酸乙酯提取部位对肿瘤细胞增殖没有明显影响,而水提部位能促进肿瘤细胞增殖。实体瘤模型中,各给药组对小鼠移植瘤均有抑制作用,其肿瘤体积和重量都较模型组低,除LRJ小剂量组外,其余各组和模型组相比较均有显著性差异(P<0.05,P<0.01)。病理检测及原位细胞凋亡检测发现,LRJ能促进瘤组织坏死和细胞凋亡。结论蜂王浆冻干粉在体内有明显的抑制肿瘤生长的作用,其抑瘤机制与促进肿瘤组织坏死和细胞凋亡有关。     

溶血性链球菌菌体制剂肿瘤细胞疫苗对荷瘤小鼠B细胞免疫效应研究

<正>肿瘤的发生发展与机体的免疫系统息息相关,当肿瘤发生以后,机体可针对肿瘤抗原产生特异性的免疫应答,但随着肿瘤的发生发展,机体的免疫功能就受到抑制。本实验试图探究溶血性链球菌菌体制剂(OK-432)肿瘤疫苗对DBA/2荷瘤小鼠B细胞免疫效应,探讨OK-432肿瘤疫苗可能的作用机制。1材料与方法1.1瘤株和实验动物:KLN-205细胞株(DBA/2小鼠来源的肺癌细胞)购自上海爱丁堡生物科技发展有限公司。KLN-205     

氨氯地平抑制小鼠黑色素瘤高转移细胞株B16体内转移的作用及相关机制研究

目的:研究不同剂量氨氯地平抑制小鼠黑色素瘤高转移细胞株B16转移的作用,并探讨其作用机制。方法:选取64只C57BL/6J小鼠,将黑色素瘤髙转移细胞株B16接种在小鼠腹股沟皮下(2×106个/只)。将接种后的小鼠以随机数字表法分为对照组和氨氯地平高、中、低剂量治疗组,对照组小鼠仅给予0.9%氯化钠注射液;治疗组小鼠给予不同剂量的氨氯地平治疗,分别为1 mg/kg(低剂量组)、3 mg/kg(中剂量组)和10 mg/kg(高剂量组)。观察各组小鼠肿瘤生长情况及身体情况;观察各组小鼠肿瘤肺转移情况,计算肺转移的结节及肿瘤抑瘤率;采用免疫组织化学法检测各组小鼠肿瘤组织中白细胞介素8(IL-8)蛋白表达水平;采用逆转录-聚合酶链反应(RT-PCR)检测各组小鼠肿瘤组织中IL-8的信使核糖核酸(mRNA)表达水平。结果:氨氯地平对小鼠黑色素瘤高转移细胞株B16的自发性肺转移有显著的抑制作用;治疗组小鼠肿瘤组织中IL-8蛋白表达均明显减弱,且随氨氯地平剂量的增加而减弱;治疗组小鼠肿瘤组织中IL-8的mRNA的表达明显低于对照组,且IL-8的mRNA的表达随氨氯地平剂量的增加而减弱。结论:氨氯地平对小鼠黑色素瘤高转移细胞株B16有一定的抑瘤和抑制肺转移作用,其作用可能与影响IL-8的表达有关。     

Effective tumor immunity to melanoma mediated by B16F10 cancer stem cell vaccine

Although tumor vaccines have been considered a promising immunotherapy approach, therapeutic tumor vaccines are mostly disappointing in the clinic due to vaccine weak immunogenicity. Cancer stem cells (CSCs) may broaden the antigenic breadth and effectively induce the immune responses against autologous cancer cells. Here we report on the development of the B16F10 CD133⁺ CD44⁺ CSCs (B16F10 CSCs) vaccine to induce tumor immunity to melanoma in mice. Efficacy of against melanoma was evaluated by analysis of tumor growth and mouse survival. Immunogenicity was assessed by ELISA and flow cytometric assays, including serum cytokines, cytotoxic activity of NK cells and splenocytes in the immunized mice. The results showed that the B16F10 CSC vaccine resulted in tumor shrinkage and mouse lifespan extension. The cytotoxic activity and IFN-γ level were significantly increased in mice immunized with B16F10 CSC vaccine compared with the mice immunized with control vaccines. Additionally, New York esophageal squamous cell carcinoma-1, an efficient tumor associated antigen over-expressed by B16F10 CSCs, was markedly reduced in expression in melanoma tissue, suggesting decrease of CSC subpopulation due to B16F10 CSC vaccination. Collectively, the findings may represent a new powerful approach for treatment of melanoma by B16F10 CSC vaccination.     

Antimetastatic effect of an immunomodulatory arabinomannan extracted from Mycobacterium tuberculosis strain Aoyama B,Z-100, through the production of interleukin-12

In this study, the role of interleukin (IL)-12 on the antimetastatic effect of Z-100 was investigated using wild-type C57BL/6 mice or IL-12p40 knockout (IL-12p40 KO) mice inoculated with highly metastatic B16F10 melanoma. When C57BL/6 mice were inoculated with B16F10 melanoma (2x10(5) cells/mouse i.v.), Z-100 (10 mg/kg i.p.) significantly suppressed the pulmonary metastasis of B16F10 melanoma 14 d after tumor inoculation. On the other hand, the antimetastatic effect of Z-100 was not observed in IL-12p40 KO mice inoculated with B16F10 melanoma. These results indicate that IL-12 is essentially required for the appearance of the antimetastatic effect of Z-100. Since helper T (Th) 2 cell responses have been reported to have a role in tumor metastasis, the regulatory effect of Z-100 on the immune balance of Th1/Th2 cell responses was investigated. In both C57BL/6 mice and IL-12p40 KO mice bearing B16F10 melanoma, Th1 cytokine production (IL-2, interferon-gamma) was significantly suppressed as compared with those in normal mice. On the other hand, Th2 cytokine production (IL-4, IL-10) in these mice was increased. The administration of Z-100 (10 mg/kg i.p.) in C57BL/6 mice bearing B16F10 melanoma improved the balance of Th1/Th2 cell responses from the Th2-dominant state to the normal state. However, the improvement of Th1/Th2 cell responses by Z-100 was not observed in IL-12p40 KO mice bearing the same tumors. In addition, Z-100 significantly increased IL-12 production by macrophages in a concentration-dependent manner, while Z-100 significantly decreased IL-10 production by these cells in vitro. These results suggested that up-regulation of IL-12 production and down-regulation of IL-10 production by Z-100 are related to the improvement of Th1/Th2 cell responses from the Th2-dominant state to the normal state, which resulted in suppression of tumor metastasis.     

新型表位基因疫苗的构建及对小鼠黑色素瘤的影响

目的：构建以MAGE-1（161—169）为表位的癌症基因疫苗并检测其抗小鼠黑色素瘤效果。方法：构建基因疫苗pcDNA—HSP70-MAGE—l（161-169）,并免疫C57BL／6小鼠。最后一次免疫后第2周,接种小鼠黑色素瘤细胞。于肿瘤细胞接种后14d,处死全部动物,称量肿瘤的重量。采用ELISA法对小鼠血清中抗MAGE-1-IgG类抗体及小鼠原代脾淋巴细胞IFN-7释放水平进行检测。结果：pcDNA-HSP70-MAGE-1（161—169）表位基因疫苗能够成功地诱发机体产生抗MAGE-1的特异性抗体,并能在体内起到抗小鼠黑色素瘤作用,抑瘤率为40．7％。同时还能提高约3．05倍的小鼠原代脾淋巴细胞IFN-7释放量。结论：pcDNA-HSP70-MAGE-1（161-169）有望成为有效的抗小鼠黑色素瘤基因疫苗。     

Improved efficacy of therapeutic vaccination with dendritic cells pulsed with tumor cell lysate against hepatocellular carcinoma by introduction of 2 tandem repeats of microbial HSP70 peptide epitope 407-426 and OK-432

Therapeutic vaccination with dendritic cells (DCs) pulsed with tumor cell lysate vaccine (H-D) represents an attractive approach for hepatocellular carcinoma (HCC) treatment. However, the efficacy of this approach is not most satisfactory for the low levels of T helper 1 (Th1)-type cytokines secretion and weak T cell responses. In this study, in order to increase the potency of H-D, two tandem repeats of microbial HSP70 peptide epitope 407–426 (2mHSP70_407-426, M2) which has been demonstrated to be effective in enhancing DC maturation were applied. The DC vaccine (HM-D) which was HCC tumor cell lysate pulsed with M2 was developed. Nevertheless, the immunotherapeutic effect was still not satisfactory enough even some promotion was obtained. Therefore, OK-432 (OK), which is a useful anti-cancer agent and effectively in stimulating DC maturation, was introduced to HM-D. Our results demonstrated that treatment with the improved DC vaccine which was tumor cell lysate pulsed with M2 and OK (HMO-D), compared with H-D and HM-D, significantly increased cell surface markers (MHC-I and II, CD40, CD80, CD86 and CD11c) expression on DCs, enhanced Th1-type cytokines (IL-12, TNF-α and IFN-γ) production but not Th2-type cytokine (IL-5) production, induced remarkable high levels of lymphocytes proliferation and CD8⁺ cytotoxic T-lymphocyte (CTL). Furthermore, immunization with HMO-D effectively reduced tumor progression and enhanced the survival of mice with H22 tumors. Besides, we also found that the capability of M2 in inducing the Th1 cytokines was stronger than OK. In view of these results, HMO-D vaccination provided a novel immunotherapeutic approach for the treatment of HCC.     

Immunostimulatory neem leaf preparation acts as an adjuvant to enhance the efficacy of poorly immunogenic B16 melanoma surface antigen vaccine

Immunogenecity of the poorly immunogenic B16 melanoma cell surface antigen (B16MelSAg) was enhanced by combining B16MelSAg with NLP in C57BL/6 mice, as evidenced by ELISA and flow cytometry. NLP was as effective as Freund's complete and incomplete adjuvant to generate antibodies recognizing the B16MelSAg. The NLP generated antibody was a gamma globulin with a subtype of IgG1. Splenic lymphocytes from B16MelSAg+NLP treated mice proliferated more rapidly in vitro when stimulated by specific (B16MelSAg) and nonspecific (ConA) stimulators, in comparison to the proliferation detected in B16MelSAg and NLP treated groups. Vaccination of mice with B16MelSAg+NLP more efficiently prevented the growth of B16 melanoma tumor than mice immunized with B16MelSAg or NLP alone. In another experiment, the immune sera (B16MelSAg+NLP) was mixed with B16Mel tumors and injected subcutaneously into syngenic C57BL/6 mice. Tumor burden was less in mice receiving a tumor along with B16MelSAg+NLP generated immune sera than other groups. The B16MelSAg+NLP generated immune sera induced antibody dependent cellular cytotoxicity specifically towards B16Mel tumor cells in vitro. We concluded that NLP might be a potential immune adjuvant for inducing active immunity towards tumor antigens.     

Effects of Ganoderma lucidum polysaccharides peptide on tumor metastasis in mice with sleep fragmentation

In recent years, studies have shown that there is a correlation between sleep disorders and cancer, but at the present stage, the research on sleep disorders and tumor related animal models is relatively insufficient. Our research will focus on mice bearing B16 F10-luc-G5 melanoma tumor with sleep fragmentation, detecting promoting effect of sleep fragmentation(SF) on the metastasis of melanoma. At the same time, we used Ganoderma lucidum polysaccharides peptide(GL-pp, 80 mg·kg~(-1)), a component of traditional Chinese medicine Ganoderma lucidum, which has long enjoyed a good reputation at home and abroad, to observe its anti-tumor metastasis effects on B16 F10-luc-G5 mice with SF. Then we used whole proteomics to analyze the difference proteins expressed in lung tissue and compared between groups, includes mice bearing B16 F10-luc-G5, mice bearing B16 F10-luc-G5 with SF and GL-pp administered mice bearing B16 F10-luc-G5 with SF. With the analysis using bioinformatics, we found several key proteins, their genes name are Adcy9, ptk2, Yap1 and Lpin2, Per1 and Tim. And several important clusters, they are, immune system, platelet aggression, energy metabolism, cell cytoskeleton, cell adhesion and circadian rhythms. Moreover, we detected the TLR4 signal pathway and macrophage differentiation to reconfirm the results of proteomics and trying to elucidate the mechanism of SF on tumor growth and metastasis and the effects of GL-pp.     

灵芝多糖对肿瘤逃避免疫监视的拮抗作用（英文）

Recent years,our research group focused the effects of G.polysaccharides,which are extracted from fruiting body of Ganoderma lucidum,on tumor evasion from immune surveillance.The immune system in patients with tumor often fails to control tumor growth because of deficient immunogenicity of tumor cells.Deficient major histocompatibility complex(MHC)classⅠ and costimulatory molecules on malignant cells partially results in tumor evasion since antigen bond MHC and costimulatory molecules provide two signals for T cell activation.Therefore,enhancement of MHC-Ⅰ and costimulatory molecules may favor restraint of the evasion.Our study found that G.polysaccharides can increase MHC classⅠ molecules such as H-2Kb and H-2Db as well as the costimulatory molecules B7-1 and B7-2 expression on B16F10 melanoma cells at both mRNA and protein levels,and can promote lymphocyte-mediated cytotoxicity.Tumour cells produce immune suppressive factors such as interleukin 10(IL-10),transforming growth factorβ1(TGF-β1)and vascular endothelial growth factor(VEGF)that suppress the function of immune cells or induce apoptosis of immune cells.Our study also found B16F10 cell culture supernatant(B16F10-CS)suppressed lymphocyte proliferation and perforin and granzyme B production in lymphocytes after induction with phytohemagglutinin(PHA),as well as lymphocyte proliferation in the mixed lymphocyte reaction.The suppression also associated with elevated levels of immunosuppressive IL-10,TGF-β1 and VEGF in B16F10-CS.Further,the production of IL-10,TGF-β1,and VEGF in B16F10 melanoma cells and lung carcinoma LA795 cells was suppressed by G.polysaccharides at both mRNA and protein levels.On the contrary,the production of IL-2,IFN-γand TNF-αin mononuclear lymphocytes was suppressed by B16F10-CF at both the mRNA and protein levels,whereas the suppression was ameliorated by G.polysaccharides.B16F10-CS was suppressive to the viability,phagocytic activity,NO production,TNF-αproduction and activity in peritoneal macrophages while G.polysaccharides had the antagonistic effects against this suppression.Then subsequently,the plasma of patients with lung cancer suppressed proliferation,CD69 expression,and perforin and granzyme B production in lymphocytes upon activation by PHA.However,these suppressive effects were reversed by G.polysaccharides.In conclusion,G.polysaccharides can improve the nature of B16F10 cells to activate lymphocytes and antagonize immunosuppression induced by B16F10-CS in lymphocytes and macrophages.These findings indicate that G.polysaccharides can restraint tumor evasion from immune surveillance,suggesting this potential value of G.polysaccharide to facilitate cancer immunotherapy.     

小鼠黑素瘤细胞培养上清对同型小鼠淋巴细胞转铁蛋白受体CD71的抑制作用分析

目的通过检测小鼠黑色素瘤细胞(B16F10)培养上清对同型小鼠淋巴细胞活化分子CD71表达的抑制,探讨黑素瘤细胞抑制淋巴细胞活化、介导肿瘤细胞免疫逃逸的机制。方法用B16F10培养上清培养同型小鼠脾淋巴细胞(上清组),经植物血凝素活化,用流式细胞仪检测小鼠脾淋巴细胞转铁蛋白受体CD71表达水平,用RPMI1640完全培养液代替B16F10培养上清作为对照组。结果上清组培养上清培养的淋巴细胞CD71表达率为(55.41±3.70)%低于对照组的(60.92±2.02)%,差异有统计学意义(P<0.05)。结论 B16F10培养上清对淋巴细胞表达CD71具有抑制作用,可抑制淋巴细胞活化,成为免疫逃逸机制之一。