Current Opinion in Immunology最新文献

英文中文

Emerging novel therapies for steroid-refractory acute graft-versus-host disease: recent advances and future directions 类固醇难治性急性移植物抗宿主病的新疗法：最新进展和未来方向

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-26 DOI: 10.1016/j.coi.2025.102649

Yishan Ye , Wenjing Hao , Florent Malard , Mohamad Mohty

Acute graft-versus-host disease (aGVHD) is a significant complication of allogeneic hematopoietic cell transplantation (allo-HCT), characterized by immune-mediated tissue damage from donor immune cells. Standard treatment of aGVHD involves systemic corticosteroids, but many patients do not respond adequately, with 30%–50% of patients being steroid refractory (SR-aGVHD) leading to poor outcomes. This highlights the need for effective second-line therapies. Ruxolitinib, a JAK1/2 inhibitor, has emerged as a key treatment, demonstrating superior overall response rates in SR-aGVHD compared to best available therapies. However, resistance and intolerance to ruxolitinib necessitate exploring novel and combination therapies such as apraglutide, neihulizumab, and other targeted agents, which have shown promising results in clinical trials. Additionally, nonpharmacologic approaches, including microbiotherapy, mesenchymal stromal cells, or alpha-1 antitrypsin, are also being investigated for their immunomodulatory potential. The future direction is to develop personalized treatment strategies that incorporate biomarkers and diverse therapeutic modalities. The aim is to enhance disease management, aiming for sustainable control and improved quality of life in patients facing the challenges of SR-aGVHD.

急性移植物抗宿主病（aGVHD）是同种异体造血细胞移植（allo-HCT）的一种重要并发症，其特征是供体免疫细胞免疫介导的组织损伤。aGVHD的标准治疗涉及全身皮质类固醇，但许多患者没有充分的反应，30%-50%的患者是类固醇难治性（SR-aGVHD），导致预后不良。这突出了对有效的二线治疗的需求。Ruxolitinib是一种JAK1/2抑制剂，已经成为一种关键的治疗方法，与现有的最佳治疗方法相比，在SR-aGVHD中显示出更高的总缓解率。然而，对ruxolitinib的耐药和不耐受需要探索新的和联合治疗，如阿普鲁肽、奈胡单抗和其他靶向药物，这些药物在临床试验中显示出有希望的结果。此外，包括微生物疗法、间充质基质细胞或α -1抗胰蛋白酶在内的非药物疗法也在研究其免疫调节潜力。未来的方向是发展个性化的治疗策略，结合生物标志物和多样化的治疗方式。目的是加强疾病管理，旨在可持续控制和改善面临SR-aGVHD挑战的患者的生活质量。

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引用次数: 0

B-cell antigen presentation in central nervous system autoimmunity b细胞抗原在中枢神经系统自身免疫中的表现

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-25 DOI: 10.1016/j.coi.2025.102647

Carson E Moseley , Joseph J Sabatino Jr , Scott S Zamvil

The role of B cells in central nervous system (CNS) autoimmunity was initially highlighted by successful clinical trials of anti-CD20 monoclonal antibodies in multiple sclerosis (MS). Research in MS as well as in aquaporin 4 (AQP4)-IgG⁺ neuromyelitis optica (NMO) and myelin oligodendrocyte glycoprotein (MOG) antibody-associated disorder (MOGAD) has expanded our appreciation of the contribution of B cells in multiple CNS autoimmune diseases. B cells have multiple functions in the initiation and propagation of CNS autoimmunity that extend beyond autoantibody production, including bidirectional interactions with T cells via B-cell antigen presentation. A deeper understanding of the cooperation between B cells and T cells in MS, NMO, and MOGAD should permit the development of more effective therapies across CNS autoimmune disorders.

抗cd20单克隆抗体在多发性硬化症（MS）中的成功临床试验最初强调了B细胞在中枢神经系统（CNS）自身免疫中的作用。MS以及水通道蛋白4 (AQP4)-IgG+视神经脊髓炎（NMO）和髓鞘少突胶质细胞糖蛋白（MOG）抗体相关疾病（MOGAD）的研究扩大了我们对B细胞在多种中枢神经系统自身免疫性疾病中的作用的认识。B细胞在CNS自身免疫的启动和传播中具有多种功能，这些功能超出了自身抗体的产生，包括通过B细胞抗原呈递与T细胞的双向相互作用。更深入地了解B细胞和T细胞在MS、NMO和MOGAD中的合作，将有助于开发更有效的治疗中枢神经系统自身免疫性疾病的方法。

引用次数: 0

From metabolomics to transfusion-associated immunomodulation 从代谢组学到输血相关免疫调节

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-22 DOI: 10.1016/j.coi.2025.102646

Angelo D’Alessandro , James C Zimring

Purpose of review

This review summarizes recent advances in metabolomics that have enhanced our understanding of transfusion-related immunomodulation (TRIM), highlighting how biochemical changes in stored blood products — with a focus on packed red blood cells — affect recipient immune responses.

Recent findings

Metabolomics has revealed critical biochemical shifts — termed storage lesions — in blood products, notably accumulation of oxidized lipids, extracellular vesicles, and hemolysis-derived molecules, such as free heme and iron. These metabolites influence recipient immunity by triggering both inflammatory and immunosuppressive pathways, mediated through mechanisms involving redox imbalance, inflammasome activation, and modulation of immune cell metabolism. Studies underscore that the immunological outcomes of transfusions are shaped not only by storage duration but also by donor-specific metabolic profiles influenced by genetics, diet, and environmental exposures. Metabolic profiling has identified novel biomarkers, such as hypoxanthine and kynurenine, which correlate with transfusion quality and immunological impact.

Summary

Metabolomics has transformed our understanding of TRIM, emphasizing that transfusion is an active biochemical intervention rather than passive fluid replacement. Moving forward, integrating metabolomic insights into transfusion medicine promises personalized strategies — selecting blood units based on metabolic rather than chronological age and donor characteristics — thus improving safety and clinical outcomes in transfusion recipients.

本文综述了代谢组学的最新进展，这些进展增强了我们对输血相关免疫调节（TRIM）的理解，重点介绍了储存血液制品中的生化变化（重点是填充红细胞）如何影响受体免疫反应。代谢组学最近的发现揭示了血液制品中关键的生化变化-称为储存病变，特别是氧化脂质，细胞外囊泡和溶血衍生分子（如游离血红素和铁）的积累。这些代谢物通过触发炎症和免疫抑制途径影响受体免疫，介导的机制包括氧化还原失衡、炎性体激活和免疫细胞代谢调节。研究强调，输血的免疫学结果不仅受储存时间的影响，还受受遗传、饮食和环境暴露影响的供者特异性代谢谱的影响。代谢分析已经确定了新的生物标志物，如次黄嘌呤和犬尿氨酸，它们与输血质量和免疫影响相关。代谢组学改变了我们对TRIM的理解，强调输血是一种主动的生化干预，而不是被动的液体替代。展望未来，将代谢组学见解整合到输血医学中有望实现个性化策略——根据代谢而不是实际年龄和献血者特征选择血液单位——从而提高输血接受者的安全性和临床结果。

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引用次数: 0

Recent progress in understanding of allergic transfusion reaction 过敏性输血反应的最新研究进展

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-20 DOI: 10.1016/j.coi.2025.102644

Fumiya Hirayama , Ayumu Kuroishi , Nobuki Matsuyama , Kazuta Yasui , Yoshihiro Takihara

Allergic transfusion reactions (ATRs) are among the most common adverse nonhemolytic transfusion reactions. However, since ATR is diagnosed based only on clinical observations, contrary to other allergic diseases, the causal relationship between a given ATR and the corresponding transfusion remains ambiguous in most cases. Although the prevailing theory suggests that immunoglobulin E (IgE)-mediated type I allergies are the primary cause of ATRs, the IgE-mediated pathway has rarely been demonstrated. Furthermore, despite accumulating reports suggesting the role of allergic predispositions to food and inhaled antigens, the etiology of ATR has yet to be fully elucidated. The recent introduction of the basophil activation test (BAT) and passive immune BAT into transfusion medicine has provided novel insights into these issues.

过敏性输血反应（ATRs）是最常见的不良非溶血性输血反应之一。然而，由于ATR的诊断仅基于临床观察，与其他过敏性疾病相反，在大多数情况下，给定ATR与相应输血之间的因果关系仍然不明确。虽然流行的理论认为免疫球蛋白E （IgE）介导的I型过敏是atr的主要原因，但IgE介导的途径很少得到证实。此外，尽管越来越多的报道表明食物过敏倾向和吸入抗原的作用，但ATR的病因尚未完全阐明。最近在输血医学中引入的嗜碱性粒细胞激活试验（BAT）和被动免疫BAT为这些问题提供了新的见解。

引用次数: 0

Microbial regulation of serotonin and neuroimmune interactions 微生物调节血清素和神经免疫相互作用

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-19 DOI: 10.1016/j.coi.2025.102639

Lewis W Yu , Elaine Y Hsiao

Bidirectional communication between the gut microbiota and neuroimmune system is essential during host–microbiome interactions. Recent research has begun to unravel microbiome–neuroimmune crosstalk and suggest classical neurochemicals as key molecular players. Serotonin, a tryptophan-derived neurochemical found across the kingdom of life, is increasingly recognized as an important effector molecule central to interkingdom communication. Here, we focus on serotonin as a key factor for microbiome–neuroimmune interaction. We briefly summarize the serotonergic system and the role of the gut microbiome in regulating serotonin bioavailability, which leads to downstream effects on neuroimmune responses and microbial fitness.

肠道微生物群和神经免疫系统之间的双向交流在宿主-微生物群相互作用中是必不可少的。最近的研究已经开始揭示微生物组-神经免疫串扰，并提出经典的神经化学物质是关键的分子参与者。5 -羟色胺是一种色氨酸衍生的神经化学物质，在生命王国中发现，越来越多的人认为它是一个重要的效应分子，在生物王国之间的交流中起着中心作用。在这里，我们将重点放在血清素作为微生物组-神经免疫相互作用的关键因素上。我们简要地总结了血清素能系统和肠道微生物组在调节血清素生物利用度中的作用，这导致了神经免疫反应和微生物适应性的下游效应。

引用次数: 0

Potential immune consequences of cold-stored platelet transfusion 冷藏血小板输注的潜在免疫后果

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-19 DOI: 10.1016/j.coi.2025.102645

Kimberly A Thomas , Rachael P Jackman

The rising interest in using cold-stored platelets (CSP) for improving outcomes in patients with active bleeding has led to multiple clinical trials with the goal of determining the in vivo hemostatic efficacy of CSP compared to standard-of-care room temperature–stored platelets. These trials are concentrated predominantly on safety and hemostatic efficacy measurements in response to therapeutic transfusion with CSP, with safety focused on the usual immune-mediated adverse reactions associated with transfusion, such as allergic and alloimmune reactions. However, given the established relationship between thrombosis and inflammation/immune activation as seen in atherosclerosis, autoimmune disease, and infection (to include the recent COVID-19 pandemic), the goal of this review is to highlight additional mechanisms by which CSP may potentiate or dampen immune activity in the context of therapeutic CSP transfusion in actively bleeding patients, thus highlighting areas of future research.

使用冷藏血小板（CSP）改善活动性出血患者预后的兴趣日益增加，导致了多项临床试验，目的是确定与标准护理室温储存血小板相比，冷藏血小板的体内止血效果。这些试验主要集中在CSP治疗性输血的安全性和止血效果测量上，安全性主要集中在与输血相关的通常免疫介导的不良反应上，如过敏反应和同种免疫反应。然而，鉴于血栓形成与炎症/免疫激活之间的既定关系，如动脉粥样硬化、自身免疫性疾病和感染（包括最近的COVID-19大流行），本综述的目的是强调CSP可能增强或抑制活动性出血患者治疗性CSP输血的免疫活性的其他机制，从而强调未来的研究领域。

引用次数: 0

SARS-CoV-2 and chronic kidney disease: challenges and future directions SARS-CoV-2与慢性肾病：挑战与未来方向

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-18 DOI: 10.1016/j.coi.2025.102642

Giannini Olivier , Elzi Luigia

Patients with chronic kidney disease (CKD), especially those with end-stage kidney disease on dialysis or kidney transplant recipients (KTRs), are highly susceptible to infections, including the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 pandemic disproportionately affected this vulnerable population, leading to increased morbidity and mortality. Immune dysfunction in CKD patients contributes to a suboptimal defense against infections and a reduced response to SARS-CoV-2 vaccinations. Although vaccination has significantly reduced severe outcomes, dialysis patients and KTRs exhibit lower seroconversion rates and faster antibody waning compared to the general population. Recent evidence suggests that booster doses improve immune responses, but vaccine efficacy remains lower in immunosuppressed individuals. This review highlights the epidemiology of COVID-19 in nephropathic patients, the mechanisms underlying their immune dysregulation, and the effectiveness of vaccination strategies. Future directions include optimizing booster regimens, integrating serological and avidity testing to tailor vaccination strategies, and exploring novel immunotherapeutic approaches. A multidisciplinary effort involving nephrologists, immunologists, and public health experts is essential to improve pandemic preparedness and develop targeted strategies to protect nephropathic patients from future viral threats.

慢性肾脏疾病（CKD）患者，特别是透析或肾移植患者（KTRs）的终末期肾脏疾病患者，极易受到感染，包括新型严重急性呼吸综合征冠状病毒2 （SARS-CoV-2）。2019冠状病毒病大流行对这一弱势群体的影响尤为严重，导致发病率和死亡率上升。CKD患者的免疫功能障碍导致对感染的防御不理想，对SARS-CoV-2疫苗的反应降低。尽管疫苗接种显著降低了严重后果，但与一般人群相比，透析患者和ktr患者表现出较低的血清转换率和更快的抗体消退。最近的证据表明，加强剂量可改善免疫反应，但疫苗效力在免疫抑制个体中仍然较低。本文综述了COVID-19在肾病患者中的流行病学、其免疫失调的机制以及疫苗接种策略的有效性。未来的方向包括优化加强方案，整合血清学和贪婪测试来定制疫苗接种策略，以及探索新的免疫治疗方法。肾病学家、免疫学家和公共卫生专家参与的多学科努力对于改善大流行防范和制定有针对性的战略以保护肾病患者免受未来病毒威胁至关重要。

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引用次数: 0

Checkpoint agonists — immunoregulatory role and its implications in the treatment of psoriasis and psoriatic arthritis 检查点激动剂-免疫调节作用及其在银屑病和银屑病关节炎治疗中的意义

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-18 DOI: 10.1016/j.coi.2025.102641

Angel Ray Baroz , Debra K Lee , Natalia Maverakis Ramirez , Smriti K Raychaudhuri , Siba P Raychaudhuri

Psoriasis and psoriatic arthritis are chronic autoimmune diseases characterized by dysregulated immune responses, particularly involving Th17 cells. Immune checkpoint molecules such as programmed death-1 (PD-1) and its ligands (PD-L1/PD-L2) are critical for maintaining immune tolerance. Disruptions in these pathways contribute to psoriatic disease pathogenesis. Notably, immune checkpoint inhibitors used in cancer therapy have been linked to the development of psoriasis or its exacerbation. This highlights the complex role of checkpoint pathways in psoriatic diseases. Thus, immune checkpoint agonists could be a therapeutic strategy aimed at restoring immune balance without widespread immunosuppression. Preclinical studies demonstrate that PD-1 agonists can mitigate inflammation by enhancing inhibitory signaling. Additionally, early-phase clinical trials in autoimmune diseases such as rheumatoid arthritis and ulcerative colitis suggest potential benefits of PD-1 modulation in psoriasis. This review explores immune checkpoint agonists in psoriatic disease as a promising alternative to conventional immunosuppressants by selectively suppressing pathogenic T-cell activity.

银屑病和银屑病关节炎是慢性自身免疫性疾病，其特征是免疫反应失调，特别是涉及Th17细胞。免疫检查点分子如程序性死亡-1 （PD-1）及其配体（PD-L1/PD-L2）对维持免疫耐受至关重要。这些通路的破坏有助于银屑病的发病机制。值得注意的是，用于癌症治疗的免疫检查点抑制剂与牛皮癣的发展或其恶化有关。这凸显了检查点通路在银屑病中的复杂作用。因此，免疫检查点激动剂可能是一种治疗策略，旨在恢复免疫平衡而不广泛的免疫抑制。临床前研究表明，PD-1激动剂可以通过增强抑制信号来减轻炎症。此外，自身免疫性疾病（如类风湿关节炎和溃疡性结肠炎）的早期临床试验表明PD-1调节在银屑病中的潜在益处。这篇综述探讨了免疫检查点激动剂在银屑病中作为一种有希望的替代传统免疫抑制剂，通过选择性地抑制致病性t细胞活性。

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Implication of epigenetic factors in development and recurrence of psoriasis 表观遗传因素在银屑病发展和复发中的意义

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-14 DOI: 10.1016/j.coi.2025.102636

Jingyi Tang, Erle Dang, Gang Wang

Psoriasis is a chronic autoimmune skin disease characterized by abnormal proliferation and differentiation of keratinocytes, with a complex pathogenesis often linked to environmental and genetic factors. Although many treatments are available, the disease still exhibits a high recurrence rate. Epigenetic regulation appears to bridge external stimuli and genetic abnormalities in the development of psoriasis. Skin-resident cells may contribute to disease recurrence through an ‘inflammatory memory’ formed through epigenetic modifications. This review focuses on skin-resident cells in psoriasis, elucidating their roles in disease progression and recurrence from an epigenetic perspective, providing scientific evidence for targeted therapies.

银屑病是一种慢性自身免疫性皮肤病，以角质形成细胞异常增殖和分化为特征，其发病机制复杂，常与环境和遗传因素有关。虽然有许多治疗方法，但这种疾病仍有很高的复发率。表观遗传调控似乎是银屑病发展过程中外部刺激和遗传异常的桥梁。皮肤驻留细胞可能通过表观遗传修饰形成的“炎症记忆”导致疾病复发。本文综述了银屑病中皮肤驻留细胞的研究进展，从表观遗传学角度阐明其在疾病进展和复发中的作用，为靶向治疗提供科学依据。

引用次数: 0

Can we cure lupus? 我们能治愈狼疮吗？

IF 5.8 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2025-08-14 DOI: 10.1016/j.coi.2025.102640

Tessa L Clement, Philip L Cohen

A general understanding of the mechanisms leading to the development of systemic lupus has emerged over recent years, yet treatment of the illness remains largely empiric and unsatisfactory. Targeted therapy with monoclonal antibodies directed against B cells and against cytokines has met limited success, as has therapy with mesenchymal and hematopoietic stem cells. In the last few years, treatment of refractory disease with chimeric-antigen reactive T cells directed against B cells (CAR-T cells) has shown unexpected promise in small patient series, with apparent long-term and complete remission of disease. Rapid progress in this area is likely to result in improved T cell and natural killer (NK) cell treatment of patients with more readily accessible and practical methods. In parallel, increased understanding of systemic lupus erythematosus disease mechanisms using systems biology and single-cell approaches is likely to uncover additional pathways to intervene in the pathogenesis of disease, raising hopes that additional options will be available for long-term treatment or cure of the disease or even prevention of disease in susceptible individuals.

近年来，人们对导致系统性狼疮发展的机制有了普遍的了解，但对这种疾病的治疗仍在很大程度上是经验和不令人满意的。针对B细胞和细胞因子的单克隆抗体靶向治疗取得了有限的成功，间充质干细胞和造血干细胞治疗也取得了有限的成功。在过去的几年里，用靶向B细胞的嵌合抗原反应性T细胞（CAR-T细胞）治疗难治性疾病在小患者系列中显示出意想不到的希望，明显的长期和完全缓解疾病。在这一领域的快速进展可能会导致改善T细胞和自然杀伤（NK）细胞治疗患者更容易获得和实用的方法。同时，利用系统生物学和单细胞方法加深对系统性红斑狼疮疾病机制的了解，可能会发现干预疾病发病机制的其他途径，从而为长期治疗或治愈疾病甚至预防易感个体的疾病提供更多选择的希望。

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