Current Opinion in Immunology最新文献

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Role of allergen immunotherapy and biologics in allergic diseases 过敏原免疫疗法和生物制剂在过敏性疾病中的作用。

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-10-01 DOI: 10.1016/j.coi.2024.102494

Xiaoying Zhou , Elisabeth M Simonin , Youn S Jung , Stephen J Galli , Kari C Nadeau

The rise in the prevalence of allergic diseases has become a global health burden. Allergic diseases are a group of immune-mediated disorders characterized by IgE-mediated conditions resulting from a type 2 helper T cell (Th2)-skewed immune response. This review aims to comprehensively summarize recent research on the roles of allergen immunotherapy (AIT) and biologics in allergic diseases. Specifically, we review the mechanisms of AIT and biologics in modulating innate and adaptive immunity involved in allergic disease pathogenesis, as well as their safety and efficacy in the treatment of allergic diseases. We also discuss current new AIT strategies such as recombinant allergen-based vaccines and allergen extract nanoencapsulation. Further research is needed to understand immune tolerance mechanisms beyond the Th2 pathway and to characterize immunological changes in responders and nonresponders to AIT or biologics. This additional research may uncover new targets for monitoring treatment responses and developing personalized treatment strategies for allergic diseases.

过敏性疾病发病率的上升已成为全球性的健康负担。过敏性疾病是一组免疫介导的疾病，其特征是由IgE介导的2型辅助T细胞（Th2）偏斜免疫反应引起的疾病。本综述旨在全面总结过敏原免疫疗法（AIT）和生物制剂在过敏性疾病中作用的最新研究。具体来说，我们回顾了过敏原免疫疗法和生物制剂调节过敏性疾病发病机制中先天性和适应性免疫的机制，以及它们治疗过敏性疾病的安全性和有效性。我们还讨论了当前新的 AIT 策略，如基于过敏原的重组疫苗和过敏原提取物纳米封装。要了解 Th2 通路以外的免疫耐受机制，并描述对 AIT 或生物制剂有反应者和无反应者的免疫学变化，还需要进一步的研究。这些额外的研究可能会发现监测治疗反应和开发过敏性疾病个性化治疗策略的新目标。

引用次数: 0

The path ahead for understanding Toll-like receptors–driven systemic autoimmunity 了解 Toll 样受体驱动的系统性自身免疫的未来之路

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-30 DOI: 10.1016/j.coi.2024.102482

Jessica A Hamerman , Gregory M Barton

Five mammalian Toll-like receptors (TLR 3, 7, 8, 9, and 13) recognize nucleic acids (NA) and induce signals that control the function of multiple immune cell types and initiate both innate and adaptive immune responses. While these receptors enable recognition of diverse microbial threats, in some instances, they respond inappropriately to self-NA released from host cells and drive the development of autoimmune diseases. Specifically, activation of TLR7 and TLR8 by self-RNA and TLR9 by self-DNA has been linked to development of a collection of systemic autoimmune or autoinflammatory disorders, including systemic lupus erythematosus, systemic juvenile idiopathic arthritis, and macrophage activation syndrome. Here, we discuss recent progress in understanding how these receptors contribute to such diverse clinical phenotypes. We highlight how comparative studies between mice and humans have not only been beneficial in identifying key pathways relevant for disease but also reveal gaps in our understanding of disease mechanisms. We identify several challenges that we hope the field will tackle in the years ahead.

哺乳动物的五种 Toll 样受体（TLR 3、7、8、9 和 13）可识别核酸（NA）并诱导信号，从而控制多种免疫细胞类型的功能并启动先天性和适应性免疫反应。虽然这些受体能识别各种微生物威胁，但在某些情况下，它们会对宿主细胞释放的自身 NA 作出不适当的反应，并导致自身免疫性疾病的发生。具体来说，自身 RNA 激活 TLR7 和 TLR8 以及自身 DNA 激活 TLR9 与一系列系统性自身免疫或自身炎症性疾病的发生有关，包括系统性红斑狼疮、系统性幼年特发性关节炎和巨噬细胞活化综合征。在此，我们讨论了在了解这些受体如何导致这些不同临床表型方面的最新进展。我们强调了小鼠和人类之间的比较研究如何不仅有益于确定与疾病相关的关键通路，而且揭示了我们对疾病机理认识的差距。我们提出了几个挑战，希望该领域在未来几年能够解决这些挑战。

引用次数: 0

Eating for immunity: how diet shapes our defenses 吃出免疫力：饮食如何塑造我们的防御能力

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-30 DOI: 10.1016/j.coi.2024.102486

Freya Q Zhang, Jing Chen, Hao Fan

Emerging studies on the diet-immune axis have uncovered novel dietary immune regulators and identified crucial targets and pathways mediating the crosstalk between specific dietary components and diverse immune cell populations. Here, we discuss the recent discovery and mechanisms by which diet-derived components, such as vitamins, amino acids, fatty acids, and antioxidants, could impact immune cell metabolism, alter signaling pathways, and reprogram the overall cellular responses. We also note crucial considerations that need to be tackled to make these findings clinically relevant, acknowledging that our current understanding often relies on simplified models that may not adequately represent the intricate network of factors influencing the diet-immune axis at the whole organism level. Overall, our growing understanding of how diet shapes our defenses underscores the importance of lifestyle choices and illuminates the potential to fine-tune immune responses through targeted nutritional strategies, thereby fortifying the immune system and bolstering our defenses against diseases.

有关膳食-免疫轴的新兴研究发现了新的膳食免疫调节剂，并确定了介导特定膳食成分和不同免疫细胞群之间相互影响的关键靶点和途径。在此，我们将讨论最近发现的膳食成分（如维生素、氨基酸、脂肪酸和抗氧化剂）可影响免疫细胞新陈代谢、改变信号通路和重编程整体细胞反应的机制。我们还注意到，要使这些发现具有临床相关性，还需要解决一些重要的考虑因素，我们承认，我们目前的认识往往依赖于简化的模型，而这些模型可能无法充分代表在整个机体水平上影响饮食-免疫轴的错综复杂的因素网络。总之，我们对饮食如何影响我们的防御能力的认识不断加深，这强调了生活方式选择的重要性，并揭示了通过有针对性的营养策略对免疫反应进行微调的潜力，从而强化免疫系统，增强我们对疾病的防御能力。

引用次数: 0

Inflammasomes and their role in PANoptosomes 炎症体及其在泛光体中的作用

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-27 DOI: 10.1016/j.coi.2024.102489

Vinod Nadella, Thirumala-Devi Kanneganti

Inflammasomes are multiprotein signaling structures in the innate immune system that drive cell death and inflammatory responses. These protein complexes generally comprise an innate immune sensor, the adaptor protein ASC, and the inflammatory protease caspase-1. Inflammasomes are formed when a cytosolic sensor, also known as a pattern recognition receptor, senses its cognate ligand, which can include microbial components, endogenous damage/danger signals, or environmental stimuli. Inflammasome assembly leads to autoproteolytic cleavage and activation of caspase-1. This activation, in turn, induces proteolytic maturation and release of the proinflammatory cytokines interleukin (IL)-1β and IL-18, and the activation of the pore-forming molecule gasdermin D to induce cell death, known as pyroptosis. Recent studies have identified inflammasomes as integral components of larger cell death complexes, known as PANoptosomes. These PANoptosomes regulate PANoptosis, an innate immune cell death pathway initiated by innate immune sensors and driven by caspases and receptor-interacting serine/threonine protein kinases. PANoptosome assembly and activation leads to cell lysis, inflammation, and the release of proinflammatory cytokines, damage-associated molecular patterns, and alarmins. In this review, we discuss the current understanding of different inflammasomes and their role in PANoptosomes.

炎症体是先天性免疫系统中的多蛋白信号结构，可驱动细胞死亡和炎症反应。这些蛋白复合物通常由先天性免疫传感器、适配蛋白 ASC 和炎症蛋白酶 caspase-1 组成。当细胞膜传感器（也称为模式识别受体）感知到它的同源配体（可能包括微生物成分、内源性损伤/危险信号或环境刺激）时，就会形成炎症小体。炎症小体的组装会导致 caspase-1 的自蛋白分解和激活。这种活化反过来又会诱导蛋白水解成熟，释放促炎细胞因子白细胞介素（IL）-1β 和 IL-18，并激活孔形成分子 gasdermin D，诱导细胞死亡，即所谓的脓毒症。最近的研究发现，炎性体是更大的细胞死亡复合物（称为 PANoptosomes）的组成部分。PANoptosomes 是一种先天性免疫细胞死亡途径，由先天性免疫传感器启动，并由 Caspases 和与受体相互作用的丝氨酸/苏氨酸蛋白激酶驱动。PANoptosome 的组装和激活会导致细胞裂解、炎症以及促炎细胞因子、损伤相关分子模式和警戒素的释放。在这篇综述中，我们将讨论目前对不同炎性体及其在 PANoptosome 中作用的理解。

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引用次数: 0

B cell memory of Immunoglobulin E (IgE) antibody responses in allergy 过敏症中免疫球蛋白 E (IgE) 抗体反应的 B 细胞记忆

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-27 DOI: 10.1016/j.coi.2024.102488

Weslley Fernandes-Braga, Maria A Curotto de Lafaille

Immunoglobulin E (IgE)-mediated allergic diseases are driven by high-affinity allergen-specific IgE antibodies. IgE antibodies bind to Fc epsilon receptors on mast cells, prompting their degranulation and initiating inflammatory reactions upon allergen crosslinking. While most IgE-producing plasma cells have short lifespans, and IgE memory B cells are exceedingly rare, studies have indicated that non-IgE-expressing type 2–polarized IgG memory B cells serve as a reservoir of IgE memory in allergies. This review explores the B cell populations underlying IgE-mediated allergies, including the cellular and molecular processes that drive IgE class switching from non-IgE memory B cells. It highlights emerging evidence from human studies identifying type 2 IgG memory B cells as the source of pathogenic IgE in allergic responses.

免疫球蛋白 E（IgE）介导的过敏性疾病是由高亲和力的过敏原特异性 IgE 抗体引起的。IgE 抗体与肥大细胞上的 Fc epsilon 受体结合，促使肥大细胞脱颗粒，并在过敏原交联后引发炎症反应。虽然大多数产生 IgE 的浆细胞寿命很短，IgE 记忆 B 细胞也极为罕见，但研究表明，非 IgE 表达的 2 型极化 IgG 记忆 B 细胞是过敏症中的 IgE 记忆库。本综述探讨了 IgE 介导的过敏症的基础 B 细胞群，包括驱动非 IgE 记忆 B 细胞 IgE 类别转换的细胞和分子过程。它强调了人类研究中新出现的证据，即 2 型 IgG 记忆 B 细胞是过敏反应中致病性 IgE 的来源。

引用次数: 0

Epithelial sensing in allergic disease 过敏性疾病中的上皮传感

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-25 DOI: 10.1016/j.coi.2024.102490

Michael V Mandanas , Nora A Barrett

Epithelial cells provide a first line of immune defense by maintaining barrier function, orchestrating mucociliary clearance, secreting antimicrobial molecules, and generating sentinel signals to both activate innate immune cells and shape adaptive immunity. Although epithelial alarmins play a particularly important role in the initiation of type 2 inflammation in response to allergens, the mechanisms by which epithelial cells sense the environment and regulate the generation and release of alarmins have been poorly understood. Recent studies have identified new sensors and signaling pathways used by barrier epithelial cells to elicit type 2 inflammation, including a novel pathway for the release of interleukin-33 from the nucleus that depends on apoptotic signaling. These recent findings have implications in the development of allergic diseases, from atopic eczema to food allergy, rhinitis, and asthma.

上皮细胞通过维持屏障功能、协调粘膜纤毛清除、分泌抗微生物分子以及产生哨兵信号来激活先天性免疫细胞和形成适应性免疫，从而提供第一道免疫防线。虽然上皮促敏素在过敏原引发的 2 型炎症中发挥着特别重要的作用，但人们对上皮细胞感知环境并调节促敏素生成和释放的机制却知之甚少。最近的研究发现了屏障上皮细胞用于诱发 2 型炎症的新传感器和信号通路，包括从细胞核释放白细胞介素-33 的新通路，该通路依赖于细胞凋亡信号。这些最新发现对过敏性疾病（从特应性湿疹到食物过敏、鼻炎和哮喘）的发展具有重要意义。

引用次数: 0

The role of intestinal bacteria in promoting tolerance to food 肠道细菌在促进食物耐受性方面的作用

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-25 DOI: 10.1016/j.coi.2024.102492

Edward Ionescu , Cathryn R Nagler

The global prevalence of atopic diseases, including food allergy, is increasing and correlates with shifts in the commensal microbiota triggered by modern lifestyle factors. Current research focuses on the immunological mechanisms and microbial cues that regulate mucosal immunity and prevent allergic responses to food. We review the identification and characterization of novel antigen-presenting cell subsets that may be critical for the establishment and maintenance of tolerance to both food and intestinal bacteria. Microbially derived products, particularly from the Lachnospiraceae family of Clostridia, regulate intestinal homeostasis through a variety of mechanisms. Here, we highlight recent work on Clostridial metabolites and products that mediate protection against allergic responses to food.

包括食物过敏在内的特应性疾病在全球的发病率不断上升，这与现代生活方式因素引发的共生微生物群的变化有关。目前的研究重点是调节粘膜免疫和预防食物过敏反应的免疫机制和微生物线索。我们回顾了新型抗原递呈细胞亚群的鉴定和特征描述，这些亚群可能对建立和维持对食物和肠道细菌的耐受性至关重要。微生物衍生产品，尤其是来自梭状芽孢杆菌科（Lachnospiraceae）的产品，通过多种机制调节肠道平衡。在此，我们将重点介绍有关梭状芽孢杆菌代谢物和产物的最新研究成果，这些代谢物和产物可介导对食物过敏反应的保护作用。

引用次数: 0

Multilevel approaches to immunization equity 实现免疫公平的多层次方法

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-24 DOI: 10.1016/j.coi.2024.102496

Joshua TB Williams , Sean T O’Leary

Over the last 2 years, immunization disparities have surged due to a pandemic, violent conflicts, economic crises, and their disrupting effects on health care systems. This review provides a multilevel framework for understanding vaccination disparities and provides examples of work addressing disparities risk factors and building immunization equity. Readers will review the World Health Organization’s 2023 priorities for vaccination equity, learn about vaccination campaigns in conflict zones like Ukraine, identify key components to a successful COVID-19 response in Ghana, and understand Brazilian efforts to minimize stigma and champion community members to build trust in mpox vaccines and health services. These efforts will improve equity and foster flourishing among vulnerable populations.

在过去两年中，由于大流行病、暴力冲突、经济危机及其对医疗保健系统的破坏性影响，免疫差异急剧扩大。本综述为了解疫苗接种差异提供了一个多层次的框架，并提供了解决差异风险因素和建立免疫公平的工作实例。读者将回顾世界卫生组织 2023 年疫苗接种公平性的优先事项，了解乌克兰等冲突地区的疫苗接种活动，确定加纳成功应对 COVID-19 的关键要素，并了解巴西为最大限度地减少污名化和支持社区成员建立对麻风疫苗和医疗服务的信任所做的努力。这些努力将提高公平性，促进弱势群体的繁荣发展。

引用次数: 0

Epithelial barrier dysfunction, type 2 immune response, and the development of chronic inflammatory diseases 上皮屏障功能障碍、2 型免疫反应和慢性炎症性疾病的发展

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-24 DOI: 10.1016/j.coi.2024.102493

Ismail Ogulur, Yagiz Pat, Duygu Yazici, Sena Ardicli, Ozge Ardicli, Yasutaka Mitamura, Mübeccel Akdis, Cezmi A Akdis

The prevalence of many chronic noncommunicable diseases has been steadily rising over the past six decades. During this time, humans have been increasingly exposed to substances toxic for epithelial cells, including air pollutants, laundry and dishwashers, household chemicals, toothpaste, food additives, microplastics, and nanoparticles, introduced into our daily lives as part of industrialization, urbanization, and modernization. These substances disrupt the epithelial barriers and lead to microbial dysbiosis and cause immune response to allergens, opportunistic pathogens, bacterial toxins, and autoantigens followed by chronic inflammation due to epigenetic mechanisms. Recent evidence from studies on the mechanisms of epithelial barrier damage has demonstrated that even trace amounts of toxic substances can damage epithelial barriers and induce tissue inflammation. Further research in this field is essential for our understanding of the causal substances and molecular mechanisms involved in the initiation of leaky epithelial barriers that cascade into chronic inflammatory diseases.

过去六十年来，许多慢性非传染性疾病的发病率持续上升。在此期间，人类越来越多地接触到对上皮细胞有毒的物质，包括空气污染物、洗衣机和洗碗机、家用化学品、牙膏、食品添加剂、微塑料和纳米粒子，这些物质随着工业化、城市化和现代化的进程被引入到我们的日常生活中。这些物质破坏了上皮屏障，导致微生物菌群失调，引起对过敏原、机会性病原体、细菌毒素和自身抗原的免疫反应，并在表观遗传机制的作用下引发慢性炎症。最近关于上皮屏障损伤机制的研究证据表明，即使是微量的有毒物质也会损伤上皮屏障并诱发组织炎症。要了解上皮屏障渗漏引发慢性炎症性疾病的致病物质和分子机制，就必须在这一领域开展进一步的研究。

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引用次数: 0

Metabolic footprint and logic through the T cell life cycle T 细胞生命周期中的代谢足迹和逻辑。

IF 6.6 2区医学 Q1 IMMUNOLOGY

Current Opinion in Immunology

Pub Date : 2024-09-21 DOI: 10.1016/j.coi.2024.102487

Tingting Fan, Rushil Shah, Ruoning Wang

A simple definition of life is a system that can self-replicate (proliferation) and self-sustain (metabolism). At the cellular level, metabolism has evolved to drive proliferation, which requires energy and building blocks to duplicate cellular biomass before division. T lymphocytes (or T cells) are required for adaptive immune responses, protecting us against invading and malignant agents capable of hyper-replication. To gain a competitive advantage over these agents, activated T cells can duplicate their biomass and divide into two daughter cells in as short as 2–6 hours, considered the fastest cell division among all cell types in vertebrates. Thus, the primary task of cellular metabolism has evolved to commit available resources to drive T cell hyperproliferation. Beyond that, the T cell life cycle involves an ordered series of fate-determining events that drive cells to transition between discrete cell states. At the life stages not involved in hyperproliferation, T cells engage metabolic programs that are more flexible to sustain viability and maintenance and sometimes are fine-tuned to support specific cellular activities. Here, we focus on the central carbon metabolism, which is most relevant to cell proliferation. We provide examples of how the changes in the central carbon metabolism may or may not change the fate of T cells and further explore a few conceptual frameworks, such as metabolic flexibility, the Goldilocks Principle, overflow metabolism, and effector-signaling metabolites, in the context of T cell fate transitions.

生命的一个简单定义是一个能够自我复制（增殖）和自我维持（新陈代谢）的系统。在细胞层面，新陈代谢的进化是为了推动增殖，增殖需要能量和构建模块，以便在分裂前复制细胞生物量。T淋巴细胞（或T细胞）是适应性免疫反应所必需的，它保护我们免受能够过度复制的入侵和恶性病原体的侵袭。为了获得对这些病原体的竞争优势，活化的 T 细胞可以在短短 2-6 小时内复制其生物量并分裂成两个子细胞，这被认为是脊椎动物所有细胞类型中最快的细胞分裂。因此，细胞新陈代谢的主要任务是将可用资源用于驱动 T 细胞的过度增殖。除此之外，T 细胞的生命周期涉及一系列有序的命运决定事件，这些事件驱动细胞在不同的细胞状态之间转换。在不涉及细胞过度增殖的生命阶段，T 细胞的新陈代谢程序更加灵活，以维持细胞的存活和维持，有时还会进行微调，以支持特定的细胞活动。在这里，我们重点讨论与细胞增殖最相关的中心碳代谢。我们举例说明了中心碳代谢的变化可能会也可能不会改变 T 细胞的命运，并结合 T 细胞的命运转变进一步探讨了一些概念框架，如代谢灵活性、金发姑娘原则、溢出代谢和效应信号代谢物。

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