{"title":"B121:检查点抑制剂疫苗刺激抗肿瘤t细胞阻断肿瘤生长","authors":"Takuya Tada, N. Landau, T. Norton","doi":"10.1158/2326-6074.CRICIMTEATIAACR18-B121","DOIUrl":null,"url":null,"abstract":"Checkpoint inhibitor therapy augments pre-existing T-cell responses to tumor antigens, resulting in tumor control in 20-40% of patients with melanoma and other cancers. As a means to increase the effectiveness of this approach, we developed a dendritic cell (DC)-based vaccine strategy that specifically induces anti-tumor T-cell responses and prevents checkpoint activation. The approach is based on lentiviral vectors that express checkpoint inhibitor and tumor antigen and transduce DCs at high efficiency as a result of virion-packaging of the lentiviral accessory protein Vpx. In addition, the vectors express CD40 ligand (CD40L), a cell surface protein that strongly activates DCs, causing the cells to mature and secrete immunostimulatory cytokines, including TNFα, IL-6, and IL-12, that potentiate T-cell responses. The therapy harnesses the ability of DCs to prime T-cell responses against tumors, resulting in long-term antigen expression and continuous, localized release of checkpoint inhibitor during antigen-presentation. In the lymphocytic choriomeningitis virus (LCMV) mouse model, immunization with DCs transduced with lentiviral vectors that express soluble programmed cell death protein 1 (PD-1), CD40L and LCMV epitopes induced a 10-fold expansion of LCMV-specific CD8 T-cells and protected the mice against high-titer LCMV and a lethal intracranial LCMV challenge. Protection was 100-fold greater than that achieved by vaccination with LCMV peptide epitope-pulsed DCs. The strategy also appeared to cure mice infected with clone 13 LCMV, a chronic form of disease that results from T-cell exhaustion induced by checkpoint activation. In the B16-OVA mouse melanoma model, immunization with DCs transduced with vectors that express soluble PD-1, CD40L and OVA epitopes or a tumor antigen epitope from tyrosinase-related protein (TRP-1) protected mice from tumor formation. DC vaccination post-B16 challenge reduced tumor growth and prolonged survival. Mice immunized four days after intravenous injection of B16 cells showed no evidence of lung melanoma nodules three weeks later. Remarkably, immunization by direct injection of lentiviral vector, a method that obviates the need to harvest patient DCs, proved equally effective as ex vivo DC transduction in suppressing tumor growth. In addition, direct injection resulted in a much longer half-life of transduced cells. These studies demonstrate the ability of this approach to induce antigen-specific responses and overcome CTL exhaustion. Moreover, the lentiviral vector approach provides a means to express tumor neoantigens for the development of personalized immunotherapies that stimulate tumor-specific T-cell responses by clones present at low level or to antigens that the host has not responded. Citation Format: Takuya Tada, Nathaniel R. Landau, Thomas David Norton. Checkpoint inhibitor vaccine stimulates antitumor T-cells that block tumor growth [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2019;7(2 Suppl):Abstract nr B121.","PeriodicalId":19329,"journal":{"name":"Novel Vaccine Platforms and Combinations","volume":"59 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Abstract B121: Checkpoint inhibitor vaccine stimulates antitumor T-cells that block tumor growth\",\"authors\":\"Takuya Tada, N. Landau, T. Norton\",\"doi\":\"10.1158/2326-6074.CRICIMTEATIAACR18-B121\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Checkpoint inhibitor therapy augments pre-existing T-cell responses to tumor antigens, resulting in tumor control in 20-40% of patients with melanoma and other cancers. As a means to increase the effectiveness of this approach, we developed a dendritic cell (DC)-based vaccine strategy that specifically induces anti-tumor T-cell responses and prevents checkpoint activation. The approach is based on lentiviral vectors that express checkpoint inhibitor and tumor antigen and transduce DCs at high efficiency as a result of virion-packaging of the lentiviral accessory protein Vpx. In addition, the vectors express CD40 ligand (CD40L), a cell surface protein that strongly activates DCs, causing the cells to mature and secrete immunostimulatory cytokines, including TNFα, IL-6, and IL-12, that potentiate T-cell responses. The therapy harnesses the ability of DCs to prime T-cell responses against tumors, resulting in long-term antigen expression and continuous, localized release of checkpoint inhibitor during antigen-presentation. In the lymphocytic choriomeningitis virus (LCMV) mouse model, immunization with DCs transduced with lentiviral vectors that express soluble programmed cell death protein 1 (PD-1), CD40L and LCMV epitopes induced a 10-fold expansion of LCMV-specific CD8 T-cells and protected the mice against high-titer LCMV and a lethal intracranial LCMV challenge. Protection was 100-fold greater than that achieved by vaccination with LCMV peptide epitope-pulsed DCs. The strategy also appeared to cure mice infected with clone 13 LCMV, a chronic form of disease that results from T-cell exhaustion induced by checkpoint activation. In the B16-OVA mouse melanoma model, immunization with DCs transduced with vectors that express soluble PD-1, CD40L and OVA epitopes or a tumor antigen epitope from tyrosinase-related protein (TRP-1) protected mice from tumor formation. DC vaccination post-B16 challenge reduced tumor growth and prolonged survival. Mice immunized four days after intravenous injection of B16 cells showed no evidence of lung melanoma nodules three weeks later. Remarkably, immunization by direct injection of lentiviral vector, a method that obviates the need to harvest patient DCs, proved equally effective as ex vivo DC transduction in suppressing tumor growth. In addition, direct injection resulted in a much longer half-life of transduced cells. These studies demonstrate the ability of this approach to induce antigen-specific responses and overcome CTL exhaustion. Moreover, the lentiviral vector approach provides a means to express tumor neoantigens for the development of personalized immunotherapies that stimulate tumor-specific T-cell responses by clones present at low level or to antigens that the host has not responded. Citation Format: Takuya Tada, Nathaniel R. Landau, Thomas David Norton. Checkpoint inhibitor vaccine stimulates antitumor T-cells that block tumor growth [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. 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引用次数: 0
摘要
检查点抑制剂疗法增强了预先存在的t细胞对肿瘤抗原的反应,使20-40%的黑色素瘤和其他癌症患者的肿瘤得到控制。为了提高这种方法的有效性,我们开发了一种基于树突状细胞(DC)的疫苗策略,该策略特异性地诱导抗肿瘤t细胞反应并阻止检查点激活。该方法基于慢病毒载体,该载体表达检查点抑制剂和肿瘤抗原,并且由于慢病毒辅助蛋白Vpx的病毒粒子包装而高效转导DCs。此外,这些载体表达CD40配体(CD40L),这是一种强烈激活dc的细胞表面蛋白,导致细胞成熟并分泌免疫刺激因子,包括TNFα、IL-6和IL-12,从而增强t细胞反应。该疗法利用dc的能力来启动t细胞对肿瘤的反应,导致长期抗原表达和抗原呈递过程中检查点抑制剂的持续、局部释放。在淋巴细胞性脉络膜脑膜炎病毒(LCMV)小鼠模型中,用表达可溶性程序性细胞死亡蛋白1 (PD-1)、CD40L和LCMV表位的慢病毒载体转导的dc进行免疫,诱导LCMV特异性CD8 t细胞扩增10倍,并保护小鼠免受高滴度LCMV和致命的颅内LCMV攻击。与接种LCMV肽表位脉冲dc相比,保护作用提高了100倍。该策略似乎也治愈了感染克隆13 LCMV的小鼠,LCMV是一种慢性疾病,由检查点激活诱导的t细胞衰竭引起。在B16-OVA小鼠黑色素瘤模型中,用表达可溶性PD-1、CD40L和OVA表位或酪氨酸酶相关蛋白(TRP-1)肿瘤抗原表位的载体转导的dc免疫可保护小鼠免于肿瘤形成。b16攻击后接种DC疫苗可减少肿瘤生长并延长生存期。静脉注射B16细胞4天后免疫的小鼠在3周后没有出现肺黑色素瘤结节的迹象。值得注意的是,通过直接注射慢病毒载体(一种无需采集患者DC的方法)进行免疫接种,在抑制肿瘤生长方面与体外DC转导同样有效。此外,直接注射导致转导细胞的半衰期更长。这些研究证明了这种方法诱导抗原特异性反应和克服CTL耗竭的能力。此外,慢病毒载体方法提供了一种表达肿瘤新抗原的方法,用于开发个性化免疫疗法,通过低水平克隆或对宿主未应答的抗原刺激肿瘤特异性t细胞反应。引用格式:Takuya Tada, Nathaniel R. Landau, Thomas David Norton。检查点抑制剂疫苗刺激抗肿瘤t细胞阻断肿瘤生长[摘要]。第四届CRI-CIMT-EATI-AACR国际癌症免疫治疗会议:将科学转化为生存;2018年9月30日至10月3日;纽约,纽约。费城(PA): AACR;癌症免疫学杂志2019;7(2增刊):摘要nr B121。
Checkpoint inhibitor therapy augments pre-existing T-cell responses to tumor antigens, resulting in tumor control in 20-40% of patients with melanoma and other cancers. As a means to increase the effectiveness of this approach, we developed a dendritic cell (DC)-based vaccine strategy that specifically induces anti-tumor T-cell responses and prevents checkpoint activation. The approach is based on lentiviral vectors that express checkpoint inhibitor and tumor antigen and transduce DCs at high efficiency as a result of virion-packaging of the lentiviral accessory protein Vpx. In addition, the vectors express CD40 ligand (CD40L), a cell surface protein that strongly activates DCs, causing the cells to mature and secrete immunostimulatory cytokines, including TNFα, IL-6, and IL-12, that potentiate T-cell responses. The therapy harnesses the ability of DCs to prime T-cell responses against tumors, resulting in long-term antigen expression and continuous, localized release of checkpoint inhibitor during antigen-presentation. In the lymphocytic choriomeningitis virus (LCMV) mouse model, immunization with DCs transduced with lentiviral vectors that express soluble programmed cell death protein 1 (PD-1), CD40L and LCMV epitopes induced a 10-fold expansion of LCMV-specific CD8 T-cells and protected the mice against high-titer LCMV and a lethal intracranial LCMV challenge. Protection was 100-fold greater than that achieved by vaccination with LCMV peptide epitope-pulsed DCs. The strategy also appeared to cure mice infected with clone 13 LCMV, a chronic form of disease that results from T-cell exhaustion induced by checkpoint activation. In the B16-OVA mouse melanoma model, immunization with DCs transduced with vectors that express soluble PD-1, CD40L and OVA epitopes or a tumor antigen epitope from tyrosinase-related protein (TRP-1) protected mice from tumor formation. DC vaccination post-B16 challenge reduced tumor growth and prolonged survival. Mice immunized four days after intravenous injection of B16 cells showed no evidence of lung melanoma nodules three weeks later. Remarkably, immunization by direct injection of lentiviral vector, a method that obviates the need to harvest patient DCs, proved equally effective as ex vivo DC transduction in suppressing tumor growth. In addition, direct injection resulted in a much longer half-life of transduced cells. These studies demonstrate the ability of this approach to induce antigen-specific responses and overcome CTL exhaustion. Moreover, the lentiviral vector approach provides a means to express tumor neoantigens for the development of personalized immunotherapies that stimulate tumor-specific T-cell responses by clones present at low level or to antigens that the host has not responded. Citation Format: Takuya Tada, Nathaniel R. Landau, Thomas David Norton. Checkpoint inhibitor vaccine stimulates antitumor T-cells that block tumor growth [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2019;7(2 Suppl):Abstract nr B121.