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Effector-Triggered Immunity. Effector-Triggered免疫力。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2023-04-26 DOI: 10.1146/annurev-immunol-101721-031732
Brenna C Remick, Moritz M Gaidt, Russell E Vance

The innate immune system detects pathogens via germline-encoded receptors that bind to conserved pathogen ligands called pathogen-associated molecular patterns (PAMPs). Here we consider an additional strategy of pathogen sensing called effector-triggered immunity (ETI). ETI involves detection of pathogen-encoded virulence factors, also called effectors. Pathogens produce effectors to manipulate hosts to create a replicative niche and/or block host immunity. Unlike PAMPs, effectors are often diverse and rapidly evolving and can thus be unsuitable targets for direct detection by germline-encoded receptors. Effectors are instead often sensed indirectly via detection of their virulence activities. ETI is a viable strategy for pathogen sensing and is used across diverse phyla, including plants, but the molecular mechanisms of ETI are complex compared to simple receptor/ligand-based PAMP detection. Here we survey the mechanisms and functions of ETI, with a particular focus on emerging insights from animal studies. We suggest that many examples of ETI may remain to be discovered, hiding in plain sight throughout immunology.

先天免疫系统通过种系编码受体检测病原体,这些受体结合到保守的病原体配体上,称为病原体相关分子模式(pathogen-associated molecular patterns, PAMPs)。在这里,我们考虑一种额外的病原体感知策略,称为效应触发免疫(ETI)。ETI涉及检测病原体编码的毒力因子,也称为效应物。病原体产生效应物操纵宿主创造复制生态位和/或阻断宿主免疫。与PAMPs不同,效应物通常是多种多样且快速进化的,因此可能不适合由种系编码受体直接检测。相反,效应物通常是通过检测其毒力活动来间接感知的。ETI是一种可行的病原体感知策略,可用于包括植物在内的多种门,但与简单的基于受体/配体的PAMP检测相比,ETI的分子机制更为复杂。在这里,我们调查了ETI的机制和功能,特别关注动物研究的新见解。我们认为许多ETI的例子可能仍有待发现,隐藏在整个免疫学的视线中。
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引用次数: 7
Biomaterials-Mediated Engineering of the Immune System. 生物材料介导的免疫系统工程。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2023-04-26 DOI: 10.1146/annurev-immunol-101721-040259
Coralie Backlund, Sasan Jalili-Firoozinezhad, Byungji Kim, Darrell J Irvine

Modulation of the immune system is an important therapeutic strategy in a wide range of diseases, and is fundamental to the development of vaccines. However, optimally safe and effective immunotherapy requires precision in the delivery of stimulatory cues to the right cells at the right place and time, to avoid toxic overstimulation in healthy tissues or incorrect programming of the immune response. To this end, biomaterials are being developed to control the location, dose, and timing of vaccines and immunotherapies. Here we discuss fundamental concepts of how biomaterials are used to enhance immune modulation, and evidence from preclinical and clinical studies of how biomaterials-mediated immune engineering can impact the development of new therapeutics. We focus on immunological mechanisms of action and in vivo modulation of the immune system, and we also discuss challenges to be overcome to speed translation of these technologies to the clinic.

免疫系统的调节是多种疾病的重要治疗策略,也是疫苗开发的基础。然而,最安全有效的免疫疗法需要在正确的地点和时间精确地将刺激信号传递给正确的细胞,以避免健康组织中的毒性过度刺激或免疫反应的错误编程。为此目的,正在开发生物材料,以控制疫苗和免疫疗法的地点、剂量和时间。在这里,我们讨论了生物材料如何用于增强免疫调节的基本概念,以及生物材料介导的免疫工程如何影响新疗法发展的临床前和临床研究的证据。我们专注于免疫作用机制和免疫系统的体内调节,我们也讨论了需要克服的挑战,以加快这些技术到临床的翻译。
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引用次数: 3
Reconciling Mouse and Human Immunology at the Altar of Genetics. 在遗传学的祭坛上调和小鼠与人类的免疫学。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2023-04-26 Epub Date: 2022-12-16 DOI: 10.1146/annurev-immunol-101721-065201
Philippe Gros, Jean-Laurent Casanova

Immunity to infection has been extensively studied in humans and mice bearing naturally occurring or experimentally introduced germline mutations. Mouse studies are sometimes neglected by human immunologists, on the basis that mice are not humans and the infections studied are experimental and not natural. Conversely, human studies are sometimes neglected by mouse immunologists, on the basis of the uncontrolled conditions of study and small numbers of patients. However, both sides would agree that the infectious phenotypes of patients with inborn errors of immunity often differ from those of the corresponding mutant mice. Why is that? We argue that this important question is best addressed by revisiting and reinterpreting the findings of both mouse and human studies from a genetic perspective. Greater caution is required for reverse-genetics studies than for forward-genetics studies, but genetic analysis is sufficiently strong to define the studies likely to stand the test of time. Genetically robust mouse and human studies can provide invaluable complementary insights into the mechanisms of immunity to infection common and specific to these two species.

人类和带有自然发生或实验性种系突变的小鼠对感染的免疫力进行了广泛的研究。人类免疫学家有时会忽视小鼠研究,理由是小鼠不是人类,所研究的感染是实验性的,不是天然的。相反,小鼠免疫学家有时也会忽视人类研究,理由是研究条件不受控制,患者人数少。不过,双方都同意,先天性免疫错误患者的感染表型往往不同于相应的突变小鼠。这是为什么呢?我们认为,要解决这一重要问题,最好从遗传学的角度重新审视和解释小鼠和人类的研究结果。与正向遗传学研究相比,反向遗传学研究需要更加谨慎,但遗传学分析足以确定哪些研究可能经得起时间的考验。基因强大的小鼠和人类研究可以提供宝贵的互补性见解,帮助人们了解这两个物种常见和特有的感染免疫机制。
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引用次数: 0
Immune Mechanisms in Inflammatory Anemia. 炎症性贫血的免疫机制。
IF 26.9 1区 医学 Q1 IMMUNOLOGY Pub Date : 2023-04-26 Epub Date: 2023-02-07 DOI: 10.1146/annurev-immunol-101320-125839
Susan P Canny, Susana L Orozco, Natalie K Thulin, Jessica A Hamerman

Maintaining the correct number of healthy red blood cells (RBCs) is critical for proper oxygenation of tissues throughout the body. Therefore, RBC homeostasis is a tightly controlled balance between RBC production and RBC clearance, through the processes of erythropoiesis and macrophage hemophagocytosis, respectively. However, during the inflammation associated with infectious, autoimmune, or inflammatory diseases this homeostatic process is often dysregulated, leading to acute or chronic anemia. In each disease setting, multiple mechanisms typically contribute to the development of inflammatory anemia, impinging on both sides of the RBC production and RBC clearance equation. These mechanisms include both direct and indirect effects of inflammatory cytokines and innate sensing. Here, we focus on common innate and adaptive immune mechanisms that contribute to inflammatory anemias using examples from several diseases, including hemophagocytic lymphohistiocytosis/macrophage activation syndrome, severe malarial anemia during Plasmodium infection, and systemic lupus erythematosus, among others.

保持健康红细胞(RBC)的正确数量对于全身组织的正常供氧至关重要。因此,红细胞稳态是通过红细胞生成和巨噬细胞噬血分别在红细胞生成和红细胞清除之间实现的严格控制的平衡。然而,在与感染性、自身免疫性或炎症性疾病相关的炎症过程中,这种平衡过程往往会失调,从而导致急性或慢性贫血。在每种疾病的情况下,多种机制通常都会导致炎症性贫血的发生,对红细胞生成和红细胞清除等式的两边都会产生影响。这些机制包括炎性细胞因子和先天感应的直接和间接影响。在此,我们将以嗜血细胞淋巴组织细胞增多症/巨噬细胞活化综合征、疟原虫感染期间的严重疟疾性贫血和系统性红斑狼疮等几种疾病为例,重点介绍导致炎症性贫血的常见先天性和适应性免疫机制。
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引用次数: 0
Molecular Mechanisms of Multimeric Assembly of IgM and IgA. IgM和IgA多聚体组装的分子机制。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2022-04-26 Epub Date: 2022-01-21 DOI: 10.1146/annurev-immunol-101320-123742
Marissa L Matsumoto

As central effectors of the adaptive immune response, immunoglobulins, or antibodies, provide essential protection from pathogens through their ability to recognize foreign antigens, aid in neutralization, and facilitate elimination from the host. Mammalian immunoglobulins can be classified into five isotypes-IgA, IgD, IgE, IgG, and IgM-each with distinct roles in mediating various aspects of the immune response. Of these isotypes, IgA and IgM are the only ones capable of multimerization, arming them with unique biological functions. Increased valency of polymeric IgA and IgM provides high avidity for binding low-affinity antigens, and their ability to be transported across the mucosal epithelium into secretions by the polymeric immunoglobulin receptor allows them to play critical roles in mucosal immunity. Here we discuss the molecular assembly, structure, and function of these multimeric antibodies.

作为适应性免疫反应的中心效应器,免疫球蛋白或抗体通过其识别外来抗原的能力提供对病原体的基本保护,帮助中和,并促进从宿主中清除。哺乳动物免疫球蛋白可分为五种同型- iga、IgD、IgE、IgG和igm -在免疫应答的各个方面发挥着不同的作用。在这些同型中,IgA和IgM是唯一能够多聚的,这使它们具有独特的生物学功能。聚合IgA和IgM价的增加提供了结合低亲和力抗原的高亲和性,并且它们通过聚合免疫球蛋白受体通过粘膜上皮运输到分泌物的能力使它们在粘膜免疫中发挥关键作用。本文讨论了这些多聚体抗体的分子组装、结构和功能。
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引用次数: 14
IL-6 Revisited: From Rheumatoid Arthritis to CAR T Cell Therapy and COVID-19. IL-6重新审视:从类风湿关节炎到CAR - T细胞治疗和COVID-19。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2022-04-26 Epub Date: 2022-02-03 DOI: 10.1146/annurev-immunol-101220-023458
Tadamitsu Kishimoto, Sujin Kang

The diverse biological activity of interleukin-6 (IL-6) contributes to the maintenance of homeostasis. Emergent infection or tissue injury induces rapid production of IL-6 and activates host defense through augmentation of acute-phase proteins and immune responses. However, excessive IL-6 production and uncontrolled IL-6 receptor signaling are critical to pathogenesis. Over the years, therapeutic agents targeting IL-6 signaling, such as tocilizumab, a humanized anti-IL-6 receptor antibody, have shown remarkable efficacy for rheumatoid arthritis, Castleman disease, and juvenile idiopathic arthritis, and their efficacy in other diseases is continually being reported. Emerging evidence has demonstrated the benefit of tocilizumab for several types of acute inflammatory diseases, including cytokine storms induced by chimeric antigen receptor T cell therapy and coronavirus disease 2019 (COVID-19). Here, we refocus attention on the biology of IL-6 and summarize the distinct pathological roles of IL-6 signaling in several acute and chronic inflammatory diseases.

白细胞介素-6 (IL-6)的多种生物活性有助于维持体内平衡。紧急感染或组织损伤诱导IL-6的快速产生,并通过增强急性期蛋白和免疫反应激活宿主防御。然而,过量的IL-6产生和不受控制的IL-6受体信号是发病的关键。多年来,靶向IL-6信号的治疗药物,如人源化抗IL-6受体抗体tocilizumab,在类风湿关节炎、Castleman病和青少年特发性关节炎中显示出显著的疗效,其在其他疾病中的疗效也不断被报道。新出现的证据表明,tocilizumab对几种类型的急性炎症性疾病有益处,包括嵌合抗原受体T细胞疗法诱导的细胞因子风暴和2019年冠状病毒病(COVID-19)。在这里,我们重新关注IL-6的生物学,并总结IL-6信号在几种急慢性炎症性疾病中的独特病理作用。
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引用次数: 32
B Cell Function in the Tumor Microenvironment. B细胞在肿瘤微环境中的功能。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2022-04-26 DOI: 10.1146/annurev-immunol-101220-015603
Stephanie M Downs-Canner, Jeremy Meier, Benjamin G Vincent, Jonathan S Serody

The tumor microenvironment (TME) is a heterogeneous, complex organization composed of tumor, stroma, and endothelial cells that is characterized by cross talk between tumor and innate and adaptive immune cells. Over the last decade, it has become increasingly clear that the immune cells in the TME play a critical role in controlling or promoting tumor growth. The function of T lymphocytes in this process has been well characterized. On the other hand, the function of B lymphocytes is less clear, although recent data from our group and others have strongly indicated a critical role for B cells in antitumor immunity. There are, however, a multitude of populations of B cells found within the TME, ranging from naive B cells all the way to terminally differentiated plasma cells and memory B cells. Here, we characterize the role of B cells in the TME in both animal models and patients, with an emphasis on dissecting how B cell heterogeneity contributes to the immune response to cancer.

肿瘤微环境(tumor microenvironment, TME)是一个由肿瘤细胞、间质细胞和内皮细胞组成的异质性复杂组织,其特征是肿瘤细胞与先天免疫细胞和适应性免疫细胞之间的串扰。在过去的十年中,越来越清楚的是,TME中的免疫细胞在控制或促进肿瘤生长方面起着关键作用。T淋巴细胞在这一过程中的作用已被很好地描述。另一方面,B淋巴细胞的功能不太清楚,尽管最近我们小组和其他人的数据强烈表明B细胞在抗肿瘤免疫中起关键作用。然而,在TME中发现了大量的B细胞群,从初始B细胞一直到终末分化的浆细胞和记忆B细胞。在这里,我们描述了B细胞在动物模型和患者的TME中的作用,重点是解剖B细胞异质性如何促进对癌症的免疫反应。
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引用次数: 58
Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection. 先天传感器触发调节细胞死亡以对抗细胞内感染。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2022-04-26 DOI: 10.1146/annurev-immunol-101320-011235
Kengo Nozaki, Lupeng Li, Edward A Miao

Intracellular pathogens pose a significant threat to animals. In defense, innate immune sensors attempt to detect these pathogens using pattern recognition receptors that either directly detect microbial molecules or indirectly detect their pathogenic activity. These sensors trigger different forms of regulated cell death, including pyroptosis, apoptosis, and necroptosis, which eliminate the infected host cell niche while simultaneously promoting beneficial immune responses. These defenses force intracellular pathogens to evolve strategies to minimize or completely evade the sensors. In this review, we discuss recent advances in our understanding of the cytosolic pattern recognition receptors that drive cell death, including NLRP1, NLRP3, NLRP6, NLRP9, NLRC4, AIM2, IFI16, and ZBP1.

细胞内病原体对动物构成重大威胁。在防御中,先天免疫传感器试图使用模式识别受体来检测这些病原体,这些模式识别受体要么直接检测微生物分子,要么间接检测其致病活性。这些传感器触发不同形式的受调节细胞死亡,包括焦亡、凋亡和坏死亡,它们消除受感染的宿主细胞生态位,同时促进有益的免疫反应。这些防御迫使细胞内病原体进化出最小化或完全逃避传感器的策略。在这篇综述中,我们讨论了驱动细胞死亡的细胞质模式识别受体的最新进展,包括NLRP1、NLRP3、NLRP6、NLRP9、NLRC4、AIM2、IFI16和ZBP1。
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引用次数: 37
The Tuberculous Granuloma and Preexisting Immunity. 结核性肉芽肿与既往免疫。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2022-04-26 Epub Date: 2022-02-07 DOI: 10.1146/annurev-immunol-093019-125148
Sara B Cohen, Benjamin H Gern, Kevin B Urdahl

Pulmonary granulomas are widely considered the epicenters of the immune response to Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). Recent animal studies have revealed factors that either promote or restrict TB immunity within granulomas. These models, however, typically ignore the impact of preexisting immunity on cellular organization and function, an important consideration because most TB probably occurs through reinfection of previously exposed individuals. Human postmortem research from the pre-antibiotic era showed that infections in Mtb-naïve individuals (primary TB) versus those with prior Mtb exposure (postprimary TB) have distinct pathologic features. We review recent animal findings in TB granuloma biology, which largely reflect primary TB. We also discuss our current understanding of postprimary TB lesions, about which much less is known. Many knowledge gaps remain, particularly regarding how preexisting immunity shapes granuloma structure and local immune responses at Mtb infection sites.

肺肉芽肿被广泛认为是对结核分枝杆菌(Mtb)免疫反应的中心,结核分枝杆菌是结核病的病原体。最近的动物研究揭示了促进或限制肉芽肿内结核病免疫的因素。然而,这些模型通常忽略了先前存在的免疫对细胞组织和功能的影响,这是一个重要的考虑因素,因为大多数结核病可能是通过先前暴露的个体的再感染发生的。前抗生素时代的人类死后研究表明,Mtb-naïve个体(原发结核)感染与先前接触结核分枝杆菌(原发结核后)的感染具有明显的病理特征。我们回顾了最近在结核病肉芽肿生物学中的动物发现,这些发现在很大程度上反映了原发性结核病。我们还讨论了我们目前对原发后结核病病变的理解,关于这一点我们知之甚少。许多知识空白仍然存在,特别是关于先前存在的免疫如何影响肉芽肿结构和结核分枝杆菌感染部位的局部免疫反应。
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引用次数: 16
Exposing T Cell Secrets Inside and Outside the Thymus. 揭露胸腺内外的T细胞秘密。
IF 29.7 1区 医学 Q1 Immunology and Microbiology Pub Date : 2022-04-26 Epub Date: 2021-12-06 DOI: 10.1146/annurev-immunol-101220-014126
Pamela J Fink

I've had serious misgivings about writing this article, because from living the experience day by day, it's hard to believe my accomplishments merit the attention. To skirt this roadblock, I forced myself to pretend I was in a conversation with my trainees, trying to distill the central driving forces of my career in science. The below chronicles my evolution from would-be astronaut/ballerina to budding developmental biologist to devoted T cell immunologist. It traces my work from a focus on intrathymic events that mold developing T cells into self-major histocompatibility complex (MHC)-restricted lymphocytes to extrathymic events that fine-tune the T cell receptor (TCR) repertoire and impose the finishing touches on T cell maturation. It is a story of a few personal attributes multiplied by generous mentors, good luck, hard work, perseverance, and knowing when to step down.

我对写这篇文章有严重的疑虑,因为从日复一日的经历来看,很难相信我的成就值得关注。为了避开这个障碍,我强迫自己假装在和我的学员交谈,试图提炼出我从事科学事业的核心驱动力。下面记录了我从未来的宇航员/芭蕾舞演员到崭露头角的发育生物学家再到献身的T细胞免疫学家的演变。它追溯了我的工作,从关注胸腺内事件,将发育中的T细胞塑造成自我主要组织相容性复合体(MHC)-限制性淋巴细胞,到胸腺外事件,微调T细胞受体(TCR)曲目,并对T细胞成熟进行最后的润色。这是一个个人特质与慷慨的导师、好运、努力工作、毅力以及知道何时退出的故事。
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引用次数: 2
期刊
Annual review of immunology
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