人树突状细胞体外直接抑瘤作用研究

目的：诱导获得人外周血树突状细胞(DCs)，研究其体外直接抑瘤作用及机制。方法：自正常人外周血分离获得单核细胞，体外rhGM-CSF和rhIL-4联合诱导培养，观察细胞形态并检测其相关表型；利用MTT法检测所诱导DCs及其培养上清对不同肿瘤细胞系的体外直接抑瘤效应。结果：诱导5—7天后的悬浮细胞具有典型的DCs形态，流式分析显示HLA-DR表达率为64．02％，CD14表达率为2．34％；抑瘤实验显示：DCs对HT29、Hela及HepG2．2．15三种肿瘤细胞系的生长具有明显抑制，其抑制率分别为20．16％，25．44％，75．41％，而对Lovo和HepG2两种肿瘤细胞系，则无明显的抑制作用。DCs培养上清均未见明显的抑瘤效应。结论：人类DCs可对某些肿瘤细胞的生长产生直接抑制作用，但对不同的肿瘤细胞其作用不同。此作用可能由DCs与肿瘤细胞的直接接触而触发，而与DCs分泌的细胞因子关系不大。     

小鼠骨髓源性树突状细胞体外诱导培养方法的比较研究

目的 探讨最佳体外诱导培养小鼠成熟树突状细胞(dendritic cells,DC)的方法.方法 分离、纯化6周龄C57BL/6小鼠骨髓单核细胞,以含10 %胎牛血清、20 ng/ml重组小鼠粒细胞-巨噬细胞集落刺激因子(GM-CSF)和10 ng/ml重组小鼠白细胞介素-4(IL-4)的RPM I-1640培养基培养7 d,然后将细胞分成对照未刺激组、肿瘤坏死因子-α(TNF-α)刺激组和TNF-α+脂多糖(lipopolysaccharides,LPS)刺激组.继续培养48 h后,观察各组细胞形态,检测IL-12、IL-6浓度及细胞表面标志CD11c、CD80、CD86 和MHC Ⅱ.结果 培养9 d后,两刺激组培养的细胞经相差显微镜观察有DC生长.TNF-α刺激组细胞培养上清液中IL-6、IL-12含量显著高于对照组(P＜0.01),但显著低于TNF-α+LPS刺激组(P＜0.05).3组均高表达CD11c,各组间无显著差异;而CD80、CD86和MHCⅡ表达阳性率TNF-α刺激组显著高于对照组(P＜0.01),TNF-α+LPS刺激组显著高于单纯TNF-α刺激组(P＜0.05).结论 联合使用TNF-α与LPS刺激可使DC成熟度提高,分泌IL-6、IL-12增加.     

GM-CSF联合α-GalCer和IL-2促进人脐带血来源iNKT细胞的增殖

目的观察GM-CSF联合α-GalCer和IL-2体外制备人脐带血来源自然杀伤T细胞(iNKT)的优势。方法采用GM-CSF联合α-GalCer和IL-2的方法体外制备iNKT细胞,与常规方法(加入α-GalCer联合IL-2)及只加IL-2进行对比,观察制备的单个核细胞的增殖情况,采用流式细胞仪检测单个核细胞中iNKT细胞、NK细胞、T细胞所占的比例,采用酶联免疫吸附试验(ELISA)测定培养上清中细胞因子IL-4和IFN-γ的浓度。结果与对照组(IL-2组)相比,GM-CSF+α-GalCer+IL-2组与α-GalCer+IL-2组均能促进iNKT细胞增殖,而前者iNKT细胞所占比例更高(P0.05);此二组与对照组(IL-2组)相比IFN-γ的浓度增高更明显(P0.05),但培养上清中IL-4的浓度增高不明显(P0.05),GM-CSF+α-GalCer+IL-2组的高于α-GalCer+IL-2组。结论 GM-CSF联合α-GalCer和IL-2体外制备的iNKT细胞增殖能力较强,有望成为一种新的更好的iNKT细胞制备方法。     

初乳中GM-CSF和IL-6含量的测定

以ELISA法检测了32例足月顺产产妇初乳中的GM-CSF和IL-6含量,结果表明初乳中GM-CSF为20-402pg/ml(28/32),IL-6含量为10-124pg/ml(23/32),为进一步研究初乳在婴幼儿免疫系统的发育、免疫功能调节过程中的作用提供了必要的理论依据.     

人脐血来源的树突状细胞的体外培养扩增

目的于体外从人脐血中培养扩增树突状细胞.方法从剖腹产胎盘中抽取脐血,分离单个核细胞,按程序加入细胞因子组合(SCF+GM-CSF+IL-4+TNF-α)进行培养及相应的鉴定.结果培养至6～7 d即出现较为典型的DC,15 d培养周期结束后,经流式细胞仪检测,所得的细胞中,CD1a的表达率为18.53%,并表达功能相关分子CD40、CD86、MHCⅡ-DR,能刺激同种T细增殖.结论利用细胞因子组合可以从脐血单个核细胞中诱导出DC,从而为下一步的临床应用研究奠定基础.     

支气管哮喘患儿TNF、IL-8和GM-CSF检测的临床意义

目的:探讨了支气管哮喘患儿血清TNF、IL-8和集落刺激因子(GM-CSF)水平的变化及临床意义。方法:应用放射免疫分析测定了32例支气管哮喘患儿血清中TNF、IL-8和GM-CSF含量,并与30名正常健康儿童作比较。结果:支气管哮喘患儿血清中TNF、IL-8和GM-CSF水平均非常显著地高于正常组(P<0.01)经一周治疗后与正常人组比较仍有显著性差异(P<0.05)。结论:观察支气管哮喘患儿血清中TNF、IL-8和GM-CSF水平的变化,对探讨其发病机理,指导临床用药具有十分重要的临床价值。     

粒细胞巨噬细胞集落刺激因子调控树突状细胞发育和功能的研究进展

树突状细胞(DC)是重要的抗原提呈细胞,专门负责抗原捕获、加工并提呈给下游T淋巴细胞从而诱导免疫应答或者免疫耐受。维持DC亚群在体内的动态平衡是保证机体免疫系统正常运转的基础。无论机体处于炎症或静息状态,粒细胞巨噬细胞集落刺激因子(GM-CSF)对DC亚群发育、分布、功能及维持DC亚群动态平衡均具有重要的调控作用。本文主要综述了GM-CSF对DC亚群发育与功能的调控作用。阐明DC发育与功能的调控机制,有助于开发新的基于DC的免疫治疗方案。     

GM-CSF对TNF-α诱导白血病细胞凋亡的抑制作用

通过TNFα以及TNFα+GM-CSF对18例白血病患者髓性白血病细胞凋亡的影响研究,发现加TNFα组凋亡细胞数明显高于TNFα+GM-CSF组,两者比较有显著性差异（P<0.01）。本结果提示TNFα有捉进肿瘤细胞凋亡作用,而 GM-CSF则可抑制这种作用。     

人外周血及脐血树突状细胞的体外分离培养

取正常人外周血或脐血,经淋巴细胞分离液分离,取中间白膜层,培养板中进行粘附,粘附细胞加培养液和细胞因子（外周血加GM－CSF和IL－4,脐血加GM－CSF和TNF－α）培养,对其形态、表型和功能分别进行鉴定和测定。结果表明约经过1周左右培养,悬浮细胞表现为典型的DC形态,带有毛刺样凸起,经DC单克隆抗体染色后用流式细胞仪测定脐血72％为DC,外周血93％为DC,并且可以刺激同种异体淋巴细胞的增殖反应。所以通过这样的不同细胞因子组合可以从人外周血和脐血中诱导培养出大量的DC细胞,为其进一步的研究奠定了基础。     

GM-CSF与IL-21基因共转染卵巢癌细胞及其对NK细胞活性的影响

 目的 探讨粒细胞巨噬细胞集落刺激因子（GM-CSF）与 IL-21 基因共转染的体外抗肿瘤效应。 方法 制备 pRSC-GM-CSF- IL21 重组质粒，再用脂质体将 质粒 pRSC-GM-CSF、pRSC-IL21 和 pRSC-GM-CSF-IL21 分别转染人卵巢癌 SKOV3 细胞（依次命名为 SKOV3/GM- CSF、SKOV3/IL21、SKOV3/GM-CSF-IL21 细胞）。以 RT- PCR 方法检测 GM-CSF 与 IL-21 表达；倒置相差显微镜观察各组细胞形态学变化；噻唑蓝法测定各组细胞增殖活性；流式细胞仪检测各组细胞细胞周期分布，细胞表面 HLA-ABC、主要组织相容性复合体 I 类相关基因（MIC A/B）、细胞间黏附分子 1（ICAM-1）的表达，以及各组细胞培养上清液对 NK 细胞活性的影响。以未转染的 SKOV3 细胞和转染空质粒 pRSC 的细胞（SKOV3/Neo）为对照。 结果 经酶切与测序鉴定，pRSC-GM-CSF-IL21 重组体构建正确，共转染 SKOV3 细胞中有目的基因 GM-CSF、IL-21 的表达。各组细胞的形态学、增殖特性、细胞周期分布及 HLA-ABC 表达无明显变化。SKOV3、SKOV3/Neo、SKOV3/GM-CSF、SKOV3/IL21 和 SKOV3/GM-CSF-IL21 细胞的 MIC A/B 表达量分别为 19.24% ± 2.31%、31.11% ± 3.76%、37.27% ± 3.04%、54.97% ± 4.77% 和 63.94% ± 5.90%；ICAM-1 表达量分别为 35.88% ± 3.06%、37.75% ± 4.09%、68.59% ± 4.84%、78.53% ± 5.78% 和 84.10% ± 3.98%；加入各组细胞培养上清液后 NK 细胞活性分别为 31.8% ± 3.6%、42.7% ± 3.3%、54.7% ± 7.4%、55.9% ± 4.4% 及 63.4% ± 6.4%。SKOV3/GM-CSF-IL21 细胞分别与 SKOV3、SKOV3/ Neo 细胞比较，3 项指标的差异均有统计学意义（P < 0.01）。 结论 GM-CSF 与 IL-21 基因共转染可上调 SKOV3 细胞表面 MIC A/B 与 ICAM-1 表达，表达产物可增强 NK 细胞活性，这有助于免疫细胞激活，增强抗肿瘤效应。     

IFN-alpha promotes definitive maturation of dendritic cells generated by short-term culture of monocytes with GM-CSF and IL-4

Dendritic cells (DC) generated in vitro have to be viable and phenotypically mature to be capable of inducing T cell-mediated immunity after in vivo administration. To facilitate optimization of DC-based vaccination protocols, we investigated whether the cytokine environment and the mode of activation affect maturation and survival of DC derived from monocytes by a short-term protocol. Monocytes cultured for 24 h with granulocyte macrophage-colony stimulating factor and interleukin-4 were stimulated with proinflammatory mediators for another 36 h to generate mature DC. Additional activation with CD40 ligand and interferon (IFN)-gamma increased viability of DC and promoted definitive maturation as defined by maintenance of a mature phenotype after withdrawal of cytokines. Addition of IFN-alpha to DC cultures prior to stimulation further enhanced definitive maturation: IFN-alpha-primed DC expressed high levels of costimulatory molecules and CC chemokine receptor 7 (CCR7) up to 5 days after cytokine withdrawal. Compared with unprimed DC, IFN-alpha-primed DC displayed equal capacity to migrate upon CCR7 ligation and to prime antigen-specific T helper cell as well as cytolytic T cell responses. In conclusion, we show that optimal maturation and survival of monocyte-derived DC require multiple activation signals. Furthermore, we identified a novel role for IFN-alpha in DC development: IFN-alpha priming of monocytes promotes definitive maturation of DC upon activation.     

雷帕霉素和地塞米松对小鼠树突状细胞分化成熟的调控

目的：观察雷帕霉素（rapamycin，Rap）和地塞米松（dexamethasone，Dex）对堵养的小鼠骨髓来源的树突状细胞（DC）分化发育的影响。方法：（1）用GM-CSF＋IL-4定向诱导C57BL／6小鼠骨髓细胞分化为DC，分别加入Rap或Dex，然后用脂多糖（LPS）刺激。在倒置显微镜和扫描电镜下，动态观察DC形态学E的变化。（2）通过流式细胞术（荧光抗体双标记法）测定CD11c^＋细胞的比例及CD86和MHC-Ⅱ类分子表达的变化。（3）通过单向混合淋巴细胞反应（MLR）观察，Rap和Dex处理的DC刺激BALB／c小鼠同种异基因T细胞增殖的情况。结果：（1）经Rap和Dex处理后，DC在形态学上呈现稳定不成熟状态。（2）Rap处理的细胞表面CDIlc和MHC-Ⅱ类分子的表达仅有轻度降低，而CD86的表达明显降低。Dex处理的细胞表面CDIlc的表达与Dex的剂量呈负相关，CD86和MHC-Ⅱ类分子的表达均明硅降低。两种药物处理的DC均可抵抗LPS的促成熟作用。（3）MLR的结果显示，Rap和Dex处理的DC刺激同种异基因BALB／c小鼠T细胞增殖的能力均较低。结论：Rap和Dex均可使DC处于稳定的不成熟状态。与Dex相比，Rap对骨髓造血F细胞向DC分化的过程影响较小，而且在抑制DC表面协同刺激分子CD86表达的同时，对MHC-Ⅱ类分子的表达影响较小。     

Salmonella enterica serovar typhimurium-induced maturation of bone marrow-derived dendritic cells

Murine bone marrow-derived dendritic cells (DC) can phagocytose and process Salmonella enterica serovar Typhimurium for peptide presentation on major histocompatibility complex class I (MHC-I) and MHC-II molecules. To investigate if a serovar Typhimurium encounter with DC induces maturation and downregulates their ability to present antigens from subsequently encountered bacteria, DC were pulsed with serovar Typhimurium 24 h prior to coincubating with Escherichia coli expressing the model antigen Crl-OVA. Quantitating presentation of OVA epitopes contained within Crl-OVA showed that Salmonella-pulsed DC had a reduced capacity to process Crl-OVA-expressing E. coli for OVA(257-264)/K(b) and OVA(265-277)/I-A(b) presentation. In addition, time course studies of DC pulsed with Crl-OVA-expressing serovar Typhimurium showed that OVA(257-264)/K(b) complexes could stimulate CD8OVA T-hybridoma cells for <24 h following a bacterial pulse, while OVA(265-277)/I-A(b) complexes could stimulate OT4H T-hybridoma cells for >24 but <48 h. The phoP-phoQ virulence locus of serovar Typhimurium also influenced the ability of DC to process Crl-OVA-expressing serovar Typhimurium for OVA(265-277)/I-A(b) presentation but not for OVA(257-264)/K(b) presentation. Furthermore, pulsing of DC with serovar Typhimurium followed by incubation for 24 or 48 h altered surface expression of MHC-I, MHC-II, CD40, CD54, CD80, and CD86, generating a DC population with a uniform, high expression level of these molecules. Finally, neither the serovar Typhimurium phoP-phoQ locus nor lipopolysaccharides (LPS) containing lipid A modifications purified from phoP mutant strains had a different effect on DC maturation from that of wild-type serovar Typhimurium or purified wild-type LPS. Thus, these data show that Salmonella or Salmonella LPS induces maturation of DC and that this process is not altered by the Salmonella phoP virulence locus. However, phoP did influence OVA(265-277)/I-A(b) presentation by DC infected with Crl-OVA-expressing serovar Typhimurium when quantitated after 2 h of bacterial infection.     

激活核受体PXR 促进小鼠GM-CSF 来源的树突状细胞的分化

目的:研究孕烷受体(PXR)激动剂pregnane-16 -carbonitrile(PCN)对小鼠GM-CSF 来源树突状细胞(DC)分化的影响。方法:建立小鼠DC 体外GM-CSF 和IL-4 诱导分化体系,并用PCN 对体系进行处理。流式细胞术检测CD11c+ DC的比例;ELISA 和流式细胞术检测DC 产生细胞因子IFN 、IL-1、IL-2 和IL-12 的量;实时荧光定量聚合酶链反应(Real-timeRT-PCR)检测调控DC 分化相关信号通路基因的表达。结果:成功建立小鼠DC 体外分化体系;PCN 处理能显著促进DC 分化,且DC 产生的细胞因子IFN 和IL-2 的量显著增多;Real-time RT-PCR 检测结果表明,与对照组相比,PCN 处理组中调控DC 分化的Notch 和Wnt 信号通路相关基因HES1、WISP1 和WISP2 的表达量显著上升。结论:PXR 激动剂PCN 能显著促进小鼠GM-CSF 来源的DC 的分化及其IFN 和IL-2 的产量,并且这种促进作用可能是通过Notch 和Wnt 信号通路进行调控。     

IL-10 prevents the differentiation of monocytes to dendritic cells but promotes their maturation to macrophages

Human monocytes cultured with granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-13 for 7 days differentiate into cells with the morphology and function of dendritic cells (DC). We have investigated the effect of IL-10 on this differentiation pathway. In the presence of IL-10 cells did not develop DC morphology, did not express CD1a and had lower levels of MHC class II. IL-10 promoted the differentiation of large cells with the morphology, cytochemistry and membrane phenotype of macrophages, including staining for nonspecific esterase and high levels of CD14, CD16 and CD68. The effect of IL-10 was dose dependent and was best appreciated when the cytokine was added at the initiation of the culture, as addition on day 3 was less inhibitory. When added to already differentiated DC on day 6, IL-10 caused only a modest reduction of MHC class II and CD1a expression, and no acquisition of the macrophage markers CD14, CD16 and CD68. Prolonged incubation up to 5 days with IL-10 did not induce a shift of differentiated DC to macrophages. On the other hand, the macrophages obtained by culturing for 7 days with GM-CSF+IL-13+IL-10 did not shift to DC upon removal of IL-10 for up to 3 days. Thus, the effect of IL-10 on monocyte differentiation, occurs only at the precursor level and confers an irreversible phenotype. From a functional point of view, cells cultured in the presence of IL-10 were poor stimulators of allogeneic cord blood T cells in mixed lymphocyte reaction (MLR) and presented tetanus toxin (TT) to specific T cell lines with much less efficiency than control DC. In contrast, IL-10-cultured DC showed 7 times greater endocytosis of FITC-dextran. This increased endocytosis was mostly mediated via the mannose receptor, as demonstrated by blocking with unlabeled mannose. In conclusion, IL-10 inhibits DC differentiation from monocytes and, in a substantial proportion of the cells, promotes the differentiation to mature macrophages. Intriguingly, IL-10 inhibits antigen presentation while it stimulates endocytic activity.     

Murine polyomavirus-like particles induce maturation of bone marrow-derived dendritic cells and proliferation of T cells

We analysed the effects of murine polyomavirus-like particles (PLPs) on bone marrow-derived dendritic cells (BMDCs) and T cells in vitro. BMDCs activated with PLPs up-regulated CD40, CD80, CD86 and major histocompatibility complex (MHC) class II surface markers and produced proinflammatory cytokines. Chimeric PLPs [expressing the ovalbumin (OVA)-peptides OVA(257-264) or OVA(323-339)], but not wildtype PLPs, activated OVA-specific CD8 T cells and OVA-specific CD4 T cells, respectively, indicating both MHC class I and II presentation of the peptides by antigen-presenting cells. Our results suggest that PLPs may be used as vaccine adjuvants priming dendritic cells to induce potent T cell responses.     

Production of IL-12, IL-23 and IL-27p28 by bone marrow-derived conventional dendritic cells rather than macrophages after LPS/TLR4-dependent induction by Salmonella Enteritidis

Induction of the interleukin-12 (IL-12) cytokine family comprising IL-12, IL-23, IL-27, and IL-12p40 by intracellular pathogens is required for orchestration of cell-mediated immune responses. Macrophages (MPhi) have been shown to be a source of IL-12 following TLR4-dependent activation by Salmonella (S.). In this study another antigen-presenting cell type, the conventional dendritic cell (cDC), was analyzed and its cytokine responses compared with those of MPhi. We generated bone marrow-derived conventional dendritic cells (BMDC) and macrophages (BMMPhi) by incubating murine bone marrow cells with supernatants containing granulocyte/macrophage colony-stimulating factor (GM-CSF) or macrophage colony-stimulating factor (M-CSF), respectively. Stimulation of BMDC and BMMPhi with S. enterica serovar Enteritidis (SE) or LPS resulted in the release of IL-12 and IL-23 by BMDC but not by BMMPhi. Furthermore, BMDC secreted approx. 20-fold more IL-12p40 and IL-27p28 than BMMPhi. However, BMDC and BMMPhi produced similar levels of IL-10. Using BMDC originating from wild-type (wt), TLR2(def) and TLR4(def) mice, we show that in BMDC the induction of IL-12, IL-23, and IL-27p28 by SE is dependent on TLR4, whereas low-level production of p40 is also mediated by pattern recognition receptors (PRR) other than TLR4. Interestingly, LPS- and SE-provoked responses of BMDC were remarkably similar indicating that LPS is the primary danger molecule of SE. Taken together, our results point to cDC rather than MPhi as the major producers of the IL-12 family members during in vitro infection with SE. The mechanisms of recognition of SE, however, appear to be the same for cDC and MPhi.     

Involvement of leptin signaling in the survival and maturation of bone marrow-derived dendritic cells

Previous studies demonstrated that lymphocyte development is impaired in leptin receptor (Ob-R)-deficient db/db mice. However, it remains unclear whether or not leptin signaling plays a physiological role in dendritic cell (DC) development and function. In this study, we first detected Ob-R expression in murine DC. Using db/db mice at a pre-diabetic stage, we demonstrate that the total number of DC generated from bone marrow (BM) cultures is significantly lower than in WT controls. Similarly, selective blockade of leptin with a soluble mouse Ob-R chimera (Ob-R:Fc) inhibited DC generation in wild-type BM cultures. The reduced DC yield in db/db BM culture was attributed to significantly increased apoptosis, which was associated with dysregulated expression of Bcl-2 family genes. Moreover, db/db DC displayed markedly reduced expression of co-stimulatory molecules and a Th2-type cytokine profile, with a poor capacity to stimulate allogeneic T cell proliferation. Consistent with their impaired DC phenotype and function, db/db DC showed significantly down-regulated activities of the PI3K/Akt pathway as well as STAT-3 and IkappaB-alpha. In conclusion, our findings demonstrate the involvement of leptin signaling in DC survival and maturation.     

骨髓问充质干细胞联合胰岛移植对受体鼠树突状细胞成熟和功能的影响

目的:研究骨髓问充质干细胞(MSCs)对骨髓细胞(BMC)分化为成熟树突状细胞(DCs),以及MSCs联合胰岛移植对受体鼠BMC来源DCs成熟和功能的影响,以探讨MSCs如何通过DCs发挥免疫抑制作用的机制.方法:将BALB/c小鼠分离纯化骨髓MSCs按比例加入C57BL/6小鼠BMC,在含重组鼠粒细胞-巨噬细胞集落刺激因子(rmGM-CSF)和重组鼠白介素4(rmIL-4)的培养条件下制备DCs,加脂多糖(LPS)促DCs成熟,检测各组DCs免疫表型的变化,抗原摄取及其分泌白细胞介素-12的能力.观察MSCs联合胰岛移植的同种异基因糖尿病模型小鼠的血糖和组织学变化,并取受体鼠BMC体外诱导为DCs,检测成熟DCs免疫表型、抗原摄取和分泌IL-12能力.结果:体内外实验证明MSCs可使BMC来源的DCs表型CD11c,成熟表面标志CD83、协同刺激分子CD86和I-A<'b>表达明显降低(P<0.05),抗原摄取和分泌IL-12能力显著下降(P<0.01).MSCs联合胰岛移植,可抑制同种异基因受体鼠免疫排斥反应的发生.结论:MSCs可通过抑制BMC来源的DCs的成熟和功能,降低DCs抗原摄取和分泌IL-12能力,诱导免疫耐受,减轻对移植胰岛的排斥反应的发生.     

gp130-linked signal transduction promotes the differentiation and maturation of dendritic cells

In order to explore the role of gp130-linked signal transduction in the differentiation and maturation of dendritic cells (DC), the mAb, B-S12, an agonist of gp130, was used for the activation of gp130 on DC. The effects of cytokines and of anti-gp130 mAb on the proliferation of DC, and their expression of IL-12 and CD80 (B7-1) by DC were evaluated. DC differentiating from peripheral blood mononuclear cells did not express the IL-6 receptor alpha chain, but expressed gp130. Anti-gp130 mAb promoted the proliferation of DC, induced by IL-4 and granulocyte macrophage colony stimulating factor (GM-CSF), by up-regulating the GM-CSF receptor on DC. DC induced by gp130 mAb and cytokines expressed DC-derived CC chemokine, as measured by RT-PCR. Induced DC also stimulated strong proliferation of autologous T cells in mixed lymphocyte reaction since an up-regulated expression of IL-12 and CD80 (B7-1) was observed in DC activated by anti-gp130 mAb. Thus, gp130 signal transduction is important for the differentiation and maturation of DC.