免疫检查点阻断(ICB)疗法

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四川大学最新Cell子刊论文:仿生纳米生物催化剂,让冷肿瘤变热,增强免疫治疗效果
生物世界· 2025-09-14 04:05
Core Viewpoint - Immunotherapy, particularly immune checkpoint blockade (ICB), has transformed cancer treatment but remains ineffective in "cold tumors" due to immune suppression in the tumor microenvironment (TME) [2][5][6] Group 1: Research Findings - A new biomimetic Ru/TiO₂ nanobiocatalyst system inspired by natural enzyme reaction systems (ERS) has been developed, capable of rapid, pH-dependent generation of reactive oxygen species (ROS) and oxygen (O₂), effectively converting cold tumors into hot tumors [3][6][7] - The Ru/TiO₂ system enhances anti-tumor immunity and suppresses tumor metastasis when used in conjunction with ICB therapy [3][7] - This research establishes a precedent for adaptive nanobiocatalysts in the TME and paves the way for the development of next-generation immunotherapies targeting drug-resistant cancers [3][6] Group 2: Mechanism of Action - The study demonstrates that Ru/TiO₂ can mediate immunogenic cell death (ICD) in melanoma cells through endoplasmic reticulum stress, while also inhibiting hypoxia-induced immune suppression [7] - The design of Ru/TiO₂ aims to reverse immune suppression and enhance immunogenicity, transforming "immune cold" tumors into "immune hot" tumors [7] Group 3: Clinical Implications - The findings suggest that the rational design of robust and efficient biocatalytic materials could extend beyond cancer treatment, opening new avenues for immune modulation in other diseases [3][6]
北京大学最新Cell子刊:激活肿瘤细胞焦亡,提高抗肿瘤免疫效果
生物世界· 2025-09-06 04:05
Core Viewpoint - Tumor immunotherapy, particularly immune checkpoint blockade (ICB) targeting the PD-1/PD-L1 pathway, shows significant promise in treating various advanced cancers, but low immune response rates hinder its efficacy and widespread application [2] Group 1: Research Findings - The study developed a self-luminous nanosystem that enhances the activation of pyroptosis in tumor cells, leading to a strong antitumor immune response when combined with anti-PD-L1 monoclonal antibodies [3][6] - Pyroptosis, a newly discovered form of immunogenic cell death (ICD), releases pro-inflammatory cytokines and damage-associated molecular patterns, triggering a robust antigen-specific immune response [5] - The self-luminous nanoparticles can emit light within the tumor without the need for an external light source, enhancing the generation of reactive oxygen species (ROS) and achieving significant tumor-killing effects [7] Group 2: Mechanism and Components - The nanosystem consists of amphiphilic porphyrin lipids, camptothecin derivatives, and a targeting moiety, which together facilitate the release of oxygen and hydrogen peroxide in the acidic tumor microenvironment [6] - The combination of chemotherapy and self-enhanced photodynamic therapy synergistically activates pyroptosis, driving immune activation that enhances the antitumor response to PD-L1 therapy [7]
西南交通大学发表最新Cell子刊论文
生物世界· 2025-08-25 10:30
免疫检查点阻断 (ICB) 疗法改变了癌症治疗格局,然而,其在胶质母细胞瘤 (GBM) 复发的临床试验中疗效有限,这在很大程度上是因为 胶质母细胞瘤的 术后肿瘤微环境 (pTME) 呈现"免疫冷肿瘤"表型,其特征为细胞毒性 T 淋巴细胞 (CTL) 浸润不足及功能受损。 2025 年 8 月 22 日,在 Cell 子刊 Cell Biomaterials 上发表了题为: Immunoregulatory hydrogel-fiber composite device as a local T cell activator for inhibiting glioblastoma recurrence 的研究论文。 我们开发了一种 水凝胶纤维复合设备 (HFCD) ,作为局部激活 细胞毒性 T 淋巴细胞 (CTL) 的手段,以增强免疫检查点阻断 (ICB) 疗法对 胶质母细胞瘤 (GBM) 复发的疗效。该设备中的水凝胶成分可调节酸性的术后肿瘤微环境 (pTME) ,为 CTL 建立有利生态位,分层结构纤维中趋化因子 CXCL10 和 PD- L1 抑制剂的定时释放可增强 CTL 浸润并维持其细胞毒性功能。在原位 ...
Cell子刊:浙江大学周民团队开发药食同源策略,增强抗肿瘤免疫的同时降低毒副作用
生物世界· 2025-08-25 08:10
Core Viewpoint - The research highlights the importance of gut microbiota in enhancing the efficacy and safety of immune checkpoint blockade (ICB) therapy for cancer treatment, proposing a novel food-medicine homologous formula to improve outcomes and reduce adverse effects [2][6][10]. Group 1: Research Development - A new oral formulation, CV/APS-MS, was developed using microcapsules to co-load Chlorella vulgaris and Astragalus polysaccharides, which are recognized for their therapeutic and nutritional benefits [3][6]. - This formulation aims to prolong retention time in the gut, nourish beneficial gut microbiota, and alleviate inflammation [6][8]. Group 2: Experimental Findings - In mouse models of melanoma lung metastasis treated with ICB therapy, CV/APS-MS improved T cell-mediated anti-tumor immunity and mitigated ICB-induced colitis and pneumonia by restoring gut microbiota balance and reducing pro-inflammatory cytokines [8][10]. - The study suggests that combining food-grade bioreagents with modern medicine could be a powerful method to enhance cancer treatment efficacy and tolerance [10].
登上Cell子刊封面,中国药科大学揭示酪氨酸激酶抑制剂通过肠道菌群增强癌症免疫疗法
生物世界· 2025-06-22 03:38
Core Viewpoint - The study highlights the role of gut microbiota, specifically the metabolite urocanic acid (UCA), in enhancing the efficacy of cancer immunotherapy when combined with tyrosine kinase inhibitors (TKIs) [3][8][11]. Group 1: Research Findings - The research demonstrates that TKIs increase the abundance of the gut bacterium Muribaculum gordoncarteri and its metabolite UCA, which enhances the response to immune checkpoint blockade (ICB) therapy [8][9]. - UCA interacts with IκBα to inhibit NF-κB activation in endothelial cells, thereby reducing the recruitment of myeloid-derived suppressor cells (MDSCs) mediated by CXCL1 [9][11]. - Higher levels of UCA and Muribaculum gordoncarteri are found in the feces of patients who respond to ICB therapy compared to non-responders, suggesting their potential as predictive biomarkers for treatment response [8][9][11]. Group 2: Implications for Cancer Treatment - The findings indicate that the interaction between TKIs and gut microbiota could be a crucial factor in improving cancer treatment outcomes, particularly for patients who currently do not respond well to existing therapies [7][9]. - Understanding the mechanisms by which UCA enhances ICB therapy could lead to new strategies for increasing the effectiveness of cancer immunotherapy [3][11].
Nature:华人团队开发新型PROTAC,治疗多种癌症类型,一作将回国加入南京大学
生物世界· 2025-05-27 03:57
Core Viewpoint - Immune checkpoint blockade (ICB) therapies, represented by anti-PD-1 and anti-PD-L1 monoclonal antibodies, have significantly transformed cancer treatment, yet many patients show poor response or develop resistance to these therapies [2][6]. Group 1: Research Findings - A study published in Nature by a team from the University of Michigan reveals that the balance between STAT5 and STAT3 shapes dendritic cell (DC) function and tumor immunity, leading to the development of a STAT3-targeting PROTAC that enhances tumor sensitivity to ICB therapy [3][10]. - The research indicates that the limited number and impaired function of dendritic cells in the tumor microenvironment (TME) hinder the effectiveness of ICB therapies, emphasizing the need to understand the mechanisms behind dendritic cell phenotype formation [6][8]. Group 2: Mechanisms of Action - STAT3 is often activated in the TME, mediating immune suppression and promoting tumor growth factors, while STAT5 is activated by cytokine signals and plays a positive role in anti-tumor immune responses [7][9]. - The study found that ICB therapy reprograms the interaction between STAT3 and STAT5 pathways in dendritic cells, activating T cell immunity and enhancing the efficacy of ICB [9][10]. Group 3: Therapeutic Implications - The development of STAT3 degradation agents, such as SD-36 and SD-2301, shows promise in reprogramming dendritic cells towards an immunogenic state, effectively treating advanced tumors and those resistant to ICB therapy without toxicity [9][10]. - This research opens new avenues for cancer immunotherapy by targeting the dynamic balance between STAT3 and STAT5 in dendritic cells [10].