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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 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。
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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 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。
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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 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。
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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 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 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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引用次数: 0
Rethinking Toll-like receptor signalling 对 Toll 样受体信号的再思考
IF 6.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-09-16 DOI: 10.1016/j.coi.2024.102460
Clare E Bryant

Since the discovery of Toll and Toll-like receptors (TLRs) in the 90s, an extensive body of research has been performed to determine how Pattern Recognition Receptors (PRRs) recognise ‘ligands’ and signal. The families of PRRs now include membrane and cytosolic proteins, which broadly signal by forming large protein platforms or supramolecular organising centres (SMOCs). The concept of SMOC-driven signalling has led to the development of a set of assumptions, particularly for TLRs, based on experimental data, to explain the physiological consequences of PRR activation. Recent research suggests that at least some of these assumptions should be reconsidered, especially as many of these receptors are important therapeutic targets for drug development, so understanding the mechanisms by which they signal is critical.

自上世纪 90 年代发现 Toll 和 Toll 样受体(Toll-like receptors,TLRs)以来,已经开展了大量研究,以确定模式识别受体(PRRs)如何识别 "配体 "并发出信号。目前,PRRs 家族包括膜蛋白和细胞膜蛋白,它们通过形成大型蛋白质平台或超分子组织中心(SMOCs)发出信号。SMOC 驱动信号的概念促使人们根据实验数据提出了一系列假设,特别是针对 TLR,以解释 PRR 激活的生理后果。最近的研究表明,至少应该重新考虑其中的一些假设,特别是因为这些受体中有许多是药物开发的重要治疗靶点,因此了解它们发出信号的机制至关重要。
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引用次数: 0
Microbiome modulation of antigen presentation in tolerance and inflammation 微生物组在耐受和炎症中对抗原递呈的调节作用
IF 6.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-09-14 DOI: 10.1016/j.coi.2024.102471
Yiming He , Gayatree Mohapatra , Sahana Asokan , Samuel Philip Nobs , Eran Elinav

The microbiome regulates mammalian immune responses from early life to adulthood. Antigen presentation, orchestrating these responses, integrates commensal and pathogenic signals. However, the temporal and spatial specificity of microbiome impacts on antigen presentation and downstream tolerance versus inflammation remain incompletely understood. Herein, we review the influences of antigen presentation of microbiome-related epitopes on immunity; impacts of microbiome-based modulation of antigen presentation on innate and adaptive immune responses; and their ramifications on homeostasis and immune-related disease, ranging from auto-inflammation to tumorigenesis. We highlight mechanisms driving these influences, such as ‘molecular mimicry’, in which microbiome auto-antigen presentation aberrantly triggers an immune response driving autoimmunity or influences conferred by microbiome-derived metabolites on antigen-presenting cells in inflammatory bowel disease. We discuss unknowns, controversies, and challenges associated with the study of microbiome regulation of antigen presentation while demonstrating how increasing knowledge may contribute to the development of microbiome-based therapeutics modulating immune responses in a variety of clinical contexts.

微生物组调节哺乳动物从幼年到成年的免疫反应。抗原递呈是这些反应的协调者,它整合了共生和致病信号。然而,微生物组对抗原递呈和下游耐受与炎症的影响在时间和空间上的特异性仍不完全清楚。在此,我们回顾了微生物组相关表位的抗原呈递对免疫的影响;基于微生物组的抗原呈递调节对先天性和适应性免疫反应的影响;以及它们对体内平衡和免疫相关疾病(从自身炎症到肿瘤发生)的影响。我们强调了这些影响的驱动机制,如 "分子模仿",即微生物组自身抗原呈递异常引发免疫反应,导致自身免疫,或微生物组衍生代谢物对炎症性肠病中抗原呈递细胞的影响。我们讨论了与微生物组调节抗原递呈研究相关的未知因素、争议和挑战,同时展示了不断增长的知识如何有助于开发基于微生物组的疗法,以调节各种临床环境中的免疫反应。
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引用次数: 0
T follicular helper cells in food allergy 食物过敏中的 T 滤泡辅助细胞
IF 6.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-09-14 DOI: 10.1016/j.coi.2024.102461
Jennifer S Chen , Donguk Lee , Uthaman Gowthaman

T follicular helper (Tfh) cells help direct the production of antibodies by B cells. In addition to promoting antibody responses to vaccination and infection, Tfh cells have been found to mediate antibody production to food antigens. Work over the past decade has delineated the specific phenotypes of Tfh cells that induce antibodies to food while also clarifying the divergent Tfh cell requirement for different food-specific antibody isotypes. Furthermore, Tfh and antibody responses to food can occur at multiple barrier sites — namely, skin, airway, and gut. Depending on the context of food antigen exposure, the immune response to food at these sites can be protective, as in the case of tolerance or immunotherapy, or pathogenic, as in the case of allergy. This review will highlight recent advances in our understanding of how Tfh cells promote antibodies to food as well as future avenues for continued discovery.

T 滤泡辅助细胞(Tfh)有助于引导 B 细胞产生抗体。除了促进对疫苗接种和感染的抗体反应外,人们还发现 Tfh 细胞能介导食物抗原抗体的产生。过去十年来的研究工作已经确定了诱导食物抗体的 Tfh 细胞的特定表型,同时也明确了不同食物特异性抗体同型的 Tfh 细胞需求。此外,对食物的 Tfh 和抗体反应可发生在多个屏障部位,即皮肤、气道和肠道。根据食物抗原暴露的具体情况,这些部位对食物的免疫反应可以是保护性的,如耐受或免疫疗法;也可以是致病性的,如过敏。本综述将重点介绍我们在了解 Tfh 细胞如何促进食物抗体方面的最新进展,以及未来继续探索的途径。
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引用次数: 0
Powerful microscopy technologies decode spatially organized cellular networks that drive response to immunotherapy in humans 强大的显微镜技术解码了驱动人体免疫疗法反应的空间组织细胞网络
IF 6.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-09-14 DOI: 10.1016/j.coi.2024.102463
Jonathan H Chen , Liad Elmelech , Alexander L Tang , Nir Hacohen

In tumors, immune cells organize into networks of different sizes and composition, including complex tertiary lymphoid structures and recently identified networks centered around the chemokines CXCL9/10/11 and CCL19. New commercially available highly multiplexed microscopy using cyclical RNA in situ hybridization and antibody-based approaches have the potential to establish the organization of the immune response in human tissue and serve as a foundation for future immunology research.

在肿瘤中,免疫细胞组织成不同大小和组成的网络,包括复杂的三级淋巴结构和最近发现的以趋化因子 CXCL9/10/11 和 CCL19 为中心的网络。使用循环 RNA 原位杂交和抗体方法的新型商用高复用显微镜有可能确定人体组织中免疫反应的组织结构,并为未来的免疫学研究奠定基础。
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引用次数: 0
Linking signal input, cell state, and spatial context to inflammatory responses 将信号输入、细胞状态和空间环境与炎症反应联系起来
IF 6.6 2区 医学 Q1 IMMUNOLOGY Pub Date : 2024-09-11 DOI: 10.1016/j.coi.2024.102462
Rachel A Gottschalk , Ronald N Germain

Signal integration is central to a causal understanding of appropriately scaled inflammatory responses. Here, we discuss recent progress in our understanding of the stimulus–response linkages downstream of pro-inflammatory inputs, with special attention to (1) the impact of cell state on the specificity of evoked gene expression and (2) the critical role of the spatial context of stimulus exposure. Advances in these directions are emerging from new tools for inferring cell–cell interactions and the activities of cytokines and transcription factors in complex microenvironments, enabling analysis of signal integration in tissue settings. Building on data-driven elucidation of factors driving inflammatory outcomes, mechanistic modeling can then contribute to a quantitative understanding of regulatory events that balance protective versus pathological inflammation.

信号整合是理解适当规模炎症反应因果关系的核心。在这里,我们将讨论最近在了解促炎症输入下游的刺激-反应联系方面取得的进展,特别关注:(1)细胞状态对诱发基因表达特异性的影响;(2)刺激暴露的空间环境的关键作用。推断细胞-细胞相互作用以及细胞因子和转录因子在复杂微环境中的活动的新工具,使分析组织环境中的信号整合成为可能,从而在这些方向上取得了进展。在数据驱动的炎症结果驱动因素阐明的基础上,机理建模有助于定量了解平衡保护性炎症与病理性炎症的调控事件。
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引用次数: 0
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Current Opinion in Immunology
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