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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 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
Natural Killer Cells in the Human Uterine Mucosa. 人子宫黏膜的自然杀伤细胞。
IF 29.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2023-04-26 DOI: 10.1146/annurev-immunol-102119-075119
Victoria Male, Ashley Moffett

The presence of granulated lymphocytes in the human uterine mucosa, known as decidua during pregnancy, or endometrium otherwise, was first noted in the nineteenth century, but it was not until 1990 that these cells were identified as a type of natural killer (NK) cell. From the outset, uterine NK (uNK) cells were found to be less cytotoxic than their circulating counterparts, peripheral NK (pNK) cells. Recently, unbiased approaches have defined three subpopulations of uNK cells, all of which cluster separately from pNK cells. Here, we review the history of research into uNK cells, including their ability to interact with placental extravillous trophoblast cells and their potential role in regulating placental implantation. We go on to review more recent advances that focus on uNK cell development and heterogeneity and their potential to defend against infection and to mediate memory effects. Finally, we consider how a better understanding of these cells could be leveraged in the future to improve outcomes of pregnancy for mothers and babies.

19世纪,人们首次注意到人子宫黏膜(孕期称为蜕膜)或子宫内膜中存在颗粒状淋巴细胞,但直到1990年,这些细胞才被确定为一种自然杀伤细胞(NK)。从一开始,子宫NK (uNK)细胞就被发现比它们的循环对应体外周NK (pNK)细胞具有更低的细胞毒性。最近,无偏方法定义了uNK细胞的三个亚群,它们都与pNK细胞分开聚集。在这里,我们回顾了对uNK细胞的研究历史,包括它们与胎盘外滋养细胞相互作用的能力以及它们在调节胎盘着床中的潜在作用。我们继续回顾最近的研究进展,重点关注uNK细胞的发育和异质性,以及它们抵御感染和介导记忆效应的潜力。最后,我们考虑如何更好地了解这些细胞,可以利用在未来改善怀孕的结果,为母亲和婴儿。
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引用次数: 7
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
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 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
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 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
Sex Differences in Immunity. 免疫力的性别差异。
IF 26.9 1区 医学 Q1 IMMUNOLOGY Pub Date : 2022-04-26 Epub Date: 2022-01-05 DOI: 10.1146/annurev-immunol-101320-125133
Nicole M Wilkinson, Ho-Chung Chen, Melissa G Lechner, Maureen A Su

Strong epidemiological evidence now exists that sex is an important biologic variable in immunity. Recent studies, for example, have revealed that sex differences are associated with the severity of symptoms and mortality due to coronavirus disease 2019 (COVID-19). Despite this evidence, much remains to be learned about the mechanisms underlying associations between sex differences and immune-mediated conditions. A growing body of experimental data has made significant inroads into understanding sex-influenced immune responses. As physicians seek to provide more targeted patient care, it is critical to understand how sex-defining factors (e.g., chromosomes, gonadal hormones) alter immune responses in health and disease. In this review, we highlight recent insights into sex differences in autoimmunity; virus infection, specifically severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; and cancer immunotherapy. A deeper understanding of underlying mechanisms will allow the development of a sex-based approach to disease screening and treatment.

目前已有强有力的流行病学证据表明,性别是免疫方面的一个重要生物变量。例如,最近的研究表明,性别差异与冠状病毒病 2019(COVID-19)的症状严重程度和死亡率有关。尽管有这些证据,但关于性别差异与免疫介导疾病之间的关联机制,仍有许多知识有待了解。越来越多的实验数据在了解性别影响的免疫反应方面取得了重大进展。随着医生寻求为病人提供更有针对性的治疗,了解性别决定因素(如染色体、性腺激素)如何改变健康和疾病中的免疫反应至关重要。在这篇综述中,我们将重点介绍有关自身免疫、病毒感染(特别是严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)感染)和癌症免疫疗法中性别差异的最新见解。对潜在机制的深入了解将有助于开发基于性别的疾病筛查和治疗方法。
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引用次数: 0
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 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
Tissue Immunity in the Bladder. 膀胱组织免疫。
IF 29.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2022-04-26 DOI: 10.1146/annurev-immunol-101220-032117
Georgina S Bowyer, Kevin W Loudon, Ondrej Suchanek, Menna R Clatworthy

The bladder is a major component of the urinary tract, an organ system that expels metabolic waste and excess water, which necessitates proximity to the external environment and its pathogens. It also houses a commensal microbiome. Therefore, its tissue immunity must resist pathogen invasion while maintaining tolerance to commensals. Bacterial infection of the bladder is common, with half of women globally experiencing one or more episodes of cystitis in their lifetime. Despite this, our knowledge of bladder immunity, particularly in humans, is incomplete. Here we consider the current view of tissue immunity in the bladder, with a focus on defense against infection. The urothelium has robust immune functionality, and its defensive capabilities are supported by resident immune cells, including macrophages, dendritic cells, natural killer cells, and γδ T cells. We discuss each in turn and consider why adaptive immune responses are often ineffective in preventing recurrent infection, as well as areas of priority for future research.

膀胱是泌尿道的主要组成部分,是排出代谢废物和多余水分的器官系统,因此必须接近外部环境及其病原体。膀胱中还存在共生微生物群。因此,膀胱的组织免疫必须在抵御病原体入侵的同时保持对共生微生物的耐受性。膀胱细菌感染很常见,全球有一半女性一生中会经历一次或多次膀胱炎。尽管如此,我们对膀胱免疫(尤其是人类膀胱免疫)的了解仍不全面。在此,我们对膀胱组织免疫的现有观点进行了探讨,重点是对感染的防御。尿路上皮细胞具有强大的免疫功能,其防御能力得到常驻免疫细胞的支持,包括巨噬细胞、树突状细胞、自然杀伤细胞和 γδ T 细胞。我们将依次讨论每种免疫反应,并探讨为什么适应性免疫反应往往不能有效预防复发性感染,以及未来研究的重点领域。
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引用次数: 0
Resistance Mechanisms to Anti-PD Cancer Immunotherapy. 抗pd肿瘤免疫治疗的耐药机制
IF 29.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2022-04-26 DOI: 10.1146/annurev-immunol-070621-030155
Matthew D Vesely, Tianxiang Zhang, Lieping Chen

The transformative success of antibodies targeting the PD-1 (programmed death 1)/B7-H1 (B7 homolog 1) pathway (anti-PD therapy) has revolutionized cancer treatment. However, only a fraction of patients with solid tumors and some hematopoietic malignancies respond to anti-PD therapy, and the reason for failure in other patients is less known. By dissecting the mechanisms underlying this resistance, current studies reveal that the tumor microenvironment is a major location for resistance to occur. Furthermore, the resistance mechanisms appear to be highly heterogeneous. Here, we discuss recent human cancer data identifying mechanisms of resistance to anti-PD therapy. We review evidence for immune-based resistance mechanisms such as loss of neoantigens, defects in antigen presentation and interferon signaling, immune inhibitory molecules, and exclusion of T cells. We also review the clinical evidence for emerging mechanisms of resistance to anti-PD therapy, such as alterations in metabolism, microbiota, and epigenetics. Finally, we discuss strategies to overcome anti-PD therapy resistance and emphasize the need to develop additional immunotherapies based on the concept of normalization cancer immunotherapy.

靶向PD-1(程序性死亡1)/B7- h1 (B7同源物1)途径的抗体(抗pd治疗)的变革性成功已经彻底改变了癌症治疗。然而,只有一小部分实体瘤和一些造血恶性肿瘤患者对抗pd治疗有反应,其他患者失败的原因尚不清楚。通过剖析这种耐药性的机制,目前的研究表明肿瘤微环境是耐药性发生的主要位置。此外,抗性机制似乎是高度异质性的。在这里,我们讨论了最近的人类癌症数据识别抗pd治疗的耐药机制。我们回顾了免疫抵抗机制的证据,如新抗原的丢失、抗原呈递和干扰素信号的缺陷、免疫抑制分子和T细胞的排斥。我们还回顾了抗pd治疗耐药机制的临床证据,如代谢、微生物群和表观遗传学的改变。最后,我们讨论了克服抗pd治疗耐药的策略,并强调需要基于规范化癌症免疫治疗的概念开发额外的免疫疗法。
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引用次数: 85
Evolutionary Landscapes of Host-Virus Arms Races. 宿主-病毒军备竞赛的进化景观。
IF 29.7 1区 医学 Q1 IMMUNOLOGY Pub Date : 2022-04-26 DOI: 10.1146/annurev-immunol-072621-084422
Jeannette L Tenthorey, Michael Emerman, Harmit S Malik

Vertebrate immune systems suppress viral infection using both innate restriction factors and adaptive immunity. Viruses mutate to escape these defenses, driving hosts to counterevolve to regain fitness. This cycle recurs repeatedly, resulting in an evolutionary arms race whose outcome depends on the pace and likelihood of adaptation by host and viral genes. Although viruses evolve faster than their vertebrate hosts, their proteins are subject to numerous functional constraints that impact the probability of adaptation. These constraints are globally defined by evolutionary landscapes, which describe the fitness and adaptive potential of all possible mutations. We review deep mutational scanning experiments mapping the evolutionary landscapes of both host and viral proteins engaged in arms races. For restriction factors and some broadly neutralizing antibodies, landscapes favor the host, which may help to level the evolutionary playing field against rapidly evolving viruses. We discuss the biophysical underpinnings of these landscapes and their therapeutic implications.

脊椎动物的免疫系统通过先天限制因子和适应性免疫抑制病毒感染。病毒变异以逃避这些防御,驱使宿主反进化以恢复适应性。这种循环反复出现,导致了一场进化军备竞赛,其结果取决于宿主和病毒基因适应的速度和可能性。尽管病毒的进化速度比它们的脊椎动物宿主快,但它们的蛋白质受到许多影响适应可能性的功能限制。这些约束是由进化景观全局定义的,它描述了所有可能突变的适应性和适应潜力。我们回顾了深入的突变扫描实验,绘制了参与军备竞赛的宿主和病毒蛋白质的进化景观。对于限制因子和一些广泛中和的抗体,环境有利于宿主,这可能有助于平衡进化的竞争环境,以对抗快速进化的病毒。我们将讨论这些景观的生物物理基础及其治疗意义。
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引用次数: 17
期刊
Annual review of immunology
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