Immunotherapy advances最新文献

英文中文

Harnessing natural killer cell effector function against cancer 利用自然杀伤细胞效应功能对抗癌症

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-12-21 DOI: 10.1093/immadv/ltad031

Matthew D. Blunt, S. Khakoo

Natural killer (NK) cells are cytotoxic innate lymphoid cells that participate in anti-tumour and anti-viral immune responses. Their ability to rapidly destroy abnormal cells and to enhance the anti-cancer function of dendritic cells, CD8+ T cells and macrophages makes them an attractive target for immunotherapeutic strategies. The development of approaches which augment NK cell activation against cancer is currently under intense preclinical and clinical research and strategies include chimeric antigen receptor (CAR) NK cells, NK cell engagers, cytokines, and immune checkpoint inhibitors. In this review, we highlight recent advances in NK cell therapeutic development and discuss their potential to add to our armamentarium against cancer.

自然杀伤（NK）细胞是细胞毒性先天性淋巴细胞，参与抗肿瘤和抗病毒免疫反应。自然杀伤细胞能迅速消灭异常细胞，并增强树突状细胞、CD8+ T 细胞和巨噬细胞的抗癌功能，因此成为免疫治疗策略中极具吸引力的靶点。目前，临床前和临床研究正在大力开发增强 NK 细胞活化抗癌功能的方法，其中包括嵌合抗原受体 (CAR) NK 细胞、NK 细胞啮合剂、细胞因子和免疫检查点抑制剂。在这篇综述中，我们将重点介绍 NK 细胞疗法开发的最新进展，并讨论它们为我们的抗癌武器库增添新成员的潜力。

引用次数: 0

Strategies to overcome low MHC-I expression in paediatric and adult tumours. 克服儿童和成人肿瘤中 MHC-I 低表达的策略。

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-12-11 eCollection Date: 2024-01-01 DOI: 10.1093/immadv/ltad028

J Guillaume, A Perzolli, M Boes

Immunotherapy has made significant advancements in cancer treatments, improving patients' survival rates and quality of life. Several challenges still need to be addressed, which include the considerable fraction of incomplete curative responses in cancer patients, the development of therapy resistance by tumours, and the occurrence of adverse effects, such as inflammatory and autoimmune complications. Paediatric tumours usually exhibit lower responsiveness to immunotherapies compared to adult tumours. Although the underlying reasons are not yet fully understood, one known mechanism by which tumours avoid immune recognition is through reduced cell surface expression of major histocompatibility complex class I (MHC-I) complexes. Accordingly, the reduced presentation of neoantigens by MHC-I hinders the recognition and targeting of tumour cells by CD8+ T cells, impeding T-cell-mediated cytotoxic anti-tumour responses. MHC-I downregulation indeed often correlates with a poorer prognosis and diminished response to immunotherapy. Understanding the mechanisms underlying MHC-I downregulation in different types of paediatric and adult tumours is crucial for developing strategies to restore MHC-I expression and enhance anti-tumour immune responses. We here discuss progress in MHC-I-based immunotherapies against cancers.

免疫疗法在癌症治疗方面取得了重大进展，提高了患者的生存率和生活质量。但仍有一些挑战需要解决，其中包括癌症患者中存在相当大比例的不完全治愈反应、肿瘤产生抗药性以及出现炎症和自身免疫并发症等不良反应。与成人肿瘤相比，儿童肿瘤对免疫疗法的反应性通常较低。虽然其根本原因尚不完全清楚，但肿瘤避免免疫识别的一个已知机制是细胞表面主要组织相容性复合物 I 类（MHC-I）复合物的表达减少。因此，MHC-I 对新抗原的呈现减少，阻碍了 CD8+ T 细胞对肿瘤细胞的识别和靶向，从而阻碍了 T 细胞介导的细胞毒性抗肿瘤反应。事实上，MHC-I的下调往往与预后较差和对免疫疗法的反应减弱相关。了解不同类型儿童和成人肿瘤中 MHC-I 下调的机制对于制定恢复 MHC-I 表达和增强抗肿瘤免疫反应的策略至关重要。我们在此讨论基于 MHC-I 的癌症免疫疗法的进展。

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引用次数: 0

Janus kinase inhibitors ameliorate clinical symptoms in patients with STAT3 gain-of-function Janus激酶抑制剂可改善STAT3功能增益患者的临床症状

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-11-24 DOI: 10.1093/immadv/ltad027

Shuya Kaneko, Fumiaki Sakura, Kay Tanita, A. Shimbo, R. Nambu, Masashi Yoshida, Shuichiro Umetsu, A. Inui, Chizuru Okada, M. Tsumura, Mamiko Yamada, Hisato Suzuki, K. Kosaki, Osamu Ohara, M. Shimizu, Tomohiro Morio, Satoshi Okada, H. Kanegane

Germline gain-of-function (GOF) variants in the signal transducer and activator of transcription 3 (STAT3) gene is an inborn error of immunity presenting with autoimmunity and lymphoproliferation. Symptoms can vary widely, and no effective treatment has been established. This study investigated the efficacy of Janus kinase (JAK) inhibitors (JAKi) in patients with STAT3-GOF. Four patients were enrolled and their clinical symptoms before and after the initiation of treatment with JAKi were described. A cell stimulation assay was performed using Epstein-Barr virus transformed lymphoid cell lines (EBV-LCLs) that were derived from the patients with STAT3-GOF. The patients presented with various symptoms, and these symptoms were mostly improved after the initiation of JAKi treatment. Upon interleukin-6 stimulation, the EBV-LCLs of patients showed enhanced STAT3 phosphorylation compare with those of the EBV-LCLs of healthy controls. In conclusion, four Japanese patients with STAT3-GOF were successfully treated with JAKi. JAKi ameliorated various symptoms and therefore, the use of JAKi could be an effective treatment option for patients with STAT3-GOF.

信号转导和激活因子 3（STAT3）基因的基因功能增益（GOF）变异是一种先天性免疫错误，表现为自身免疫和淋巴细胞增殖。该病的症状千差万别，目前尚无有效的治疗方法。本研究调查了 Janus 激酶（JAK）抑制剂（JAKi）对 STAT3-GOF 患者的疗效。研究共招募了四名患者，并描述了他们在开始接受JAKi治疗前后的临床症状。使用从 STAT3-GOF 患者身上提取的 Epstein-Barr 病毒转化淋巴细胞系（EBV-LCLs）进行了细胞刺激试验。患者表现出各种症状，这些症状在开始接受 JAKi 治疗后大多得到了改善。在白细胞介素-6的刺激下，患者的EBV-LCLs与健康对照组的EBV-LCLs相比，STAT3磷酸化增强。总之，四名患有 STAT3-GOF 的日本患者成功地接受了 JAKi 治疗。JAKi改善了患者的各种症状，因此，对STAT3-GOF患者来说，使用JAKi可能是一种有效的治疗选择。

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引用次数: 0

Efficacy of PD-1 checkpoint inhibitor therapy in melanoma and beyond: are peripheral T cell phenotypes the key? PD-1检查点抑制剂治疗黑色素瘤及其他疾病的疗效:外周T细胞表型是关键吗?

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-11-22 eCollection Date: 2023-01-01 DOI: 10.1093/immadv/ltad026

Katie R Flaherty, Stephanie Kucykowicz, Johannes Schroth, Will Traves, Kyle T Mincham, George E Finney

Summary Immunotherapy treatment strategies have proven effective in a limited portion of patients, where identifying responders from non-responders to treatment remains a challenge. While some indications can be drawn from invasive biopsies, we need more accessible methods for predicting response and better correlates of response prior to starting therapy. Recent work has identified differences in immune composition at baseline in peripheral blood from melanoma patients responding to PD-1 blockade treatment. Through flow cytometric analysis of T cell receptors, phenotypical features of CD8+ and CD4+ T cells and Tregs could allow for the stratification of treatment response. Analysing T cells within peripheral blood could potentially allow for the stratification of PD-1 treatment response prior to therapy in different cancer settings.

免疫疗法治疗策略已被证明对有限部分患者有效，在这些患者中，识别对治疗有反应和无反应仍然是一个挑战。虽然可以从侵入性活检中得出一些适应症，但我们需要更容易获得的方法来预测反应，并在开始治疗之前更好地确定反应的相关性。最近的工作已经确定了对PD-1阻断治疗有反应的黑色素瘤患者外周血基线免疫组成的差异。通过T细胞受体的流式细胞术分析，CD8+和CD4+ T细胞和Tregs的表型特征可以对治疗反应进行分层。分析外周血中的T细胞可能允许在不同癌症治疗前对PD-1治疗反应进行分层。

引用次数: 0

DC-targeting Lentivectors for Cancer Immunotherapy 肿瘤免疫治疗的dc靶向慢载体

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-11-01 DOI: 10.1093/immadv/ltad023

Ester Gea-Mallorquí, Sarah Rowland-Jones

Abstract Lentivectors (LVs) induce sustained transgene expression and are attractive vaccine platforms for complex immune scenarios like cancer and persistent infections. This review summarises the literature on lentivectors with potential uses for in vivo immunotherapy, focusing on those targeting the most potent antigen-presenting cells: dendritic cells (DCs). There is a growing interest in myeloid-targeting therapies as, by influencing an early stage in the immune hierarchy, they can orchestrate a more diverse and complex targeted immune response. We dissect the nature of DC-targeting LVs and their induced immune responses to understand the state of the art, identify the knowledge gaps and guide efforts to maximise the generation of potent and effective immune responses. Lentivector-based vaccines provide several advantages over other vaccine platforms, such as directed tropism and limited vector immunogenicity, and have been shown to generate effective and sustained immune responses. Overall, DC-targeting lentivectors stand out as promising tools to be exploited in cancer immunotherapy, and new-generation LVs can further exploit the gained knowledge in the study of naturally-occurring lentiviruses for a more directed and adjuvanted response.

慢载体(LVs)诱导持续的转基因表达，是复杂免疫场景(如癌症和持续感染)有吸引力的疫苗平台。本文综述了在体内免疫治疗中具有潜在用途的慢载体的文献，重点介绍了针对最有效的抗原呈递细胞:树突状细胞(dc)的慢载体。人们对骨髓靶向治疗越来越感兴趣，因为通过影响免疫层次的早期阶段，它们可以协调更多样化和复杂的靶向免疫反应。我们剖析了dc靶向lv的性质及其诱导的免疫反应，以了解最新的技术状况，确定知识差距，并指导努力最大限度地产生有效的免疫反应。与其他疫苗平台相比，基于慢载体的疫苗具有若干优势，如定向性和有限载体免疫原性，并已证明可产生有效和持续的免疫反应。总的来说，靶向dc的慢病毒载体是癌症免疫治疗中很有前途的工具，新一代lv可以进一步利用在自然存在的慢病毒研究中获得的知识，以获得更直接和辅助的应答。

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引用次数: 0

Time to treat the climate and nature crisis as one indivisible global health emergency. 是时候将气候和自然危机视为一个不可分割的全球卫生紧急事件了。

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-10-25 eCollection Date: 2023-01-01 DOI: 10.1093/immadv/ltad021

Kamran Abbasi, Parveen Ali, Virginia Barbour, Thomas Benfield, Kirsten Bibbins-Domingo, Stephen Hancocks, Richard Horton, Laurie Laybourn-Langton, Robert Mash, Peush Sahni, Wadeia Mohammad Sharief, Paul Yonga, Chris Zielinski

引用次数: 0

NLRP3 inflammasome activation in sensory neurons promotes chronic inflammatory and osteoarthritis pain 感觉神经元中NLRP3炎性小体的激活促进慢性炎症和骨关节炎疼痛

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-10-24 DOI: 10.1093/immadv/ltad022

Patrícia Silva Santos Ribeiro, Hanneke L D M Willemen, Sabine Versteeg, Christian Martin Gil, Niels Eijkelkamp

Abstract Pain is one of the most debilitating symptoms in rheumatic diseases. Pain often persists after total knee replacement in osteoarthritis, or when inflammation is minimal/absent in rheumatoid arthritis. This suggests that pain transitions to a chronic state independent of the original damage/inflammation. Mitochondrial dysfunction in the nervous system promotes chronic pain and is linked to NLRP3 inflammasome activation. Therefore, we investigated the role of mitochondrial dysfunction and NLRP3 inflammasome activation in the transition from acute to persistent inflammation-induced nociplastic pain and in persistent monoiodoacetate-induced osteoarthritis pain. Intraplantar injection of carrageenan in mice induced transient inflammatory pain that resolved within 7 days. A subsequent intraplantar PGE2 injection induced persistent mechanical hypersensitivity, while in naive mice it resolved within one day. Thus, this initial transient inflammation induced maladaptive nociceptor neuroplasticity, so-called hyperalgesic priming. At day 7, when mice were primed, expression of NLRP3 inflammasome pathway components were increased, and dorsal root ganglia neurons displayed signs of activated NLRP3 inflammasome. Inhibition of NLRP3 inflammasome with MCC950 prevented the transition from acute to chronic pain in this hyperalgesic priming model. In mice with persistent monoiodoacetate-induced osteoarthritis pain, neurons displayed signs of mitochondrial oxidative stress and NLRP3 inflammasome activation. Blocking NLRP3 inflammasome activity attenuated established osteoarthritis pain. In males, NLPR3 inhibition had longer lasting effects than in females. Overall, these data suggest that NLRP3 inflammasome activation in sensory neurons, potentially caused by neuronal oxidative stress, promotes development of persistent inflammatory and osteoarthritis pain. Therefore, targeting NLRP3 inflammasome pathway may be a promising approach to treat chronic pain.

疼痛是风湿病中最使人衰弱的症状之一。骨关节炎患者在全膝关节置换术后，或类风湿关节炎患者炎症轻微或无炎症时，疼痛常持续存在。这表明疼痛转变为一种独立于原始损伤/炎症的慢性状态。神经系统线粒体功能障碍促进慢性疼痛，并与NLRP3炎性体激活有关。因此，我们研究了线粒体功能障碍和NLRP3炎性小体激活在从急性到持续炎症诱导的伤害性疼痛和持续单碘乙酸诱导的骨关节炎疼痛的转变中的作用。小鼠足底注射角叉菜胶可引起短暂性炎性疼痛，7天内消退。随后足底注射PGE2诱导了持续的机械过敏，而在幼稚小鼠中，它在一天内消退。因此，这种初始的短暂炎症引起了伤害感受器神经可塑性不良，即所谓的痛觉过敏启动。在第7天，当小鼠被启动时，NLRP3炎症小体通路组分的表达增加，背根神经节神经元显示NLRP3炎症小体被激活的迹象。MCC950对NLRP3炎性体的抑制阻止了痛觉过敏启动模型中由急性疼痛向慢性疼痛的转变。在持续单碘酸盐诱导的骨关节炎疼痛小鼠中，神经元表现出线粒体氧化应激和NLRP3炎性体激活的迹象。阻断NLRP3炎性体活性可减轻已建立的骨关节炎疼痛。在男性中，NLPR3抑制作用比女性持久。总的来说，这些数据表明，感觉神经元中NLRP3炎性小体的激活，可能是由神经元氧化应激引起的，促进了持续性炎症和骨关节炎疼痛的发展。因此，靶向NLRP3炎性体通路可能是治疗慢性疼痛的一种有希望的方法。

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引用次数: 0

Correction to: Blockade of innate inflammatory cytokines TNFα, IL-1β, or IL-6 overcomes virotherapy-induced cancer equilibrium to promote tumor regression. 更正：先天性炎性细胞因子TNFα、IL-1β或IL-6的阻断克服了病毒治疗诱导的癌症平衡，促进肿瘤消退。

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-10-12 eCollection Date: 2023-01-01 DOI: 10.1093/immadv/ltad019

[This corrects the article DOI: 10.1093/immadv/ltad011.].

[这更正了文章DOI:10.1093/imadv/ltad011.]。

引用次数: 0

Correction to: TIM-3: a tumor-associated antigen beyond checkpoint inhibition? 更正：TIM-3：一种超越检查点抑制的肿瘤相关抗原？

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-10-12 eCollection Date: 2023-01-01 DOI: 10.1093/immadv/ltad018

[This corrects the article DOI: 10.1093/immadv/ltac021.].

[这更正了文章DOI:10.1093/imadv/ltac021.]。

引用次数: 0

Correction to: Immunology of allergen immunotherapy. 更正：过敏原免疫疗法的免疫学。

Q2 IMMUNOLOGY

Immunotherapy advances

Pub Date : 2023-10-12 eCollection Date: 2023-01-01 DOI: 10.1093/immadv/ltad017

[This corrects the article DOI: 10.1093/immadv/ltac022.].

[这更正了文章DOI:10.1093/imadv/ltac022.]。

引用次数: 0

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全部 ACS Publications Elsevier ieeexplore Springer The Royal Society of Chemistry Wiley

期刊

Immunotherapy advances

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