Pub Date : 2024-08-30DOI: 10.1038/s41577-024-01084-8
Mayar Allam, Ahmet F. Coskun
In this Tools of the Trade article, Mayar Allam and Ahmet Coskun describe how they combined spatial metabolomics and proteomics profiling — in a framework they call scSpaMet — to explore, at the single-cell level, how metabolic profiles vary by location and in disease.
在这篇《贸易工具》（Tools of the Trade）文章中，马亚尔-阿拉姆（Mayar Allam）和艾哈迈德-科斯昆（Ahmet Coskun）介绍了他们如何将空间代谢组学和蛋白质组学分析结合起来，在他们称之为 scSpaMet 的框架内，在单细胞水平上探索代谢特征如何因位置和疾病而异。
{"title":"Combining spatial metabolomics and proteomics profiling of single cells","authors":"Mayar Allam, Ahmet F. Coskun","doi":"10.1038/s41577-024-01084-8","DOIUrl":"10.1038/s41577-024-01084-8","url":null,"abstract":"In this Tools of the Trade article, Mayar Allam and Ahmet Coskun describe how they combined spatial metabolomics and proteomics profiling — in a framework they call scSpaMet — to explore, at the single-cell level, how metabolic profiles vary by location and in disease.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142101137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-23DOI: 10.1038/s41577-024-01086-6
Kirsty Minton
Kloosterman, Erbani et al. describe a lipid-mediated, metabolic crosstalk between tumour-associated macrophages and glioblastoma cells that supports tumour growth.
{"title":"Lipid transfer from tumour-associated macrophages supports glioblastoma","authors":"Kirsty Minton","doi":"10.1038/s41577-024-01086-6","DOIUrl":"10.1038/s41577-024-01086-6","url":null,"abstract":"Kloosterman, Erbani et al. describe a lipid-mediated, metabolic crosstalk between tumour-associated macrophages and glioblastoma cells that supports tumour growth.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142042396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-23DOI: 10.1038/s41577-024-01082-w
Yvonne Bordon
Organoids generated from individuals with coeliac disease identify a role for IL-7 in disease pathogenesis.
从患有乳糜泻的患者体内生成的器官组织确定了 IL-7 在疾病发病机制中的作用。
{"title":"Organoids identify a role for IL-7 in coeliac disease","authors":"Yvonne Bordon","doi":"10.1038/s41577-024-01082-w","DOIUrl":"10.1038/s41577-024-01082-w","url":null,"abstract":"Organoids generated from individuals with coeliac disease identify a role for IL-7 in disease pathogenesis.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142042383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-09DOI: 10.1038/s41577-024-01067-9
Timothy J. Wells, Tyron Esposito, Ian R. Henderson, Larisa I. Labzin
Antibody-dependent enhancement (ADE) of infectious disease is a phenomenon whereby host antibodies increase the severity of an infection. It is well established in viral infections but ADE also has an underappreciated role during bacterial, fungal and parasitic infections. ADE can occur during both primary infections and re-infections with the same or a related pathogen; therefore, understanding the underlying mechanisms of ADE is critical for understanding the pathogenesis and progression of many infectious diseases. Here, we review the four distinct mechanisms by which antibodies increase disease severity during an infection. We discuss the most established mechanistic explanation for ADE, where cross-reactive, disease-enhancing antibodies bound to pathogens interact with Fc receptors, thereby enhancing pathogen entry or replication, ultimately increasing the total pathogen load. Additionally, we explore how some pathogenic antibodies can shield bacteria from complement-dependent killing, thereby enhancing bacterial survival. We interrogate the molecular mechanisms by which antibodies can amplify inflammation to drive severe disease, even in the absence of increased pathogen replication. We also examine emerging roles for autoantibodies in enhancing the pathogenesis of infectious diseases. Finally, we discuss how we can leverage these insights to improve vaccine design and future treatments for infectious diseases. This Review discusses the different mechanisms of antibody-dependent enhancement (ADE) of infectious disease, including how antibodies can increase the pathogen load, protect bacteria from the immune system and amplify inflammation. The authors also highlight the role of autoantibodies and consider how a better understanding of ADE can be used to improve vaccines and treatments for infectious diseases.
传染性疾病的抗体依赖性增强（ADE）是宿主抗体增加感染严重程度的一种现象。这种现象在病毒感染中已得到公认，但在细菌、真菌和寄生虫感染中，ADE 的作用也未得到充分重视。ADE 既可发生在原发感染中，也可发生在同一病原体或相关病原体的再感染中；因此，了解 ADE 的基本机制对于了解许多感染性疾病的发病机制和进展至关重要。在此，我们回顾了抗体在感染期间增加疾病严重性的四种不同机制。我们讨论了 ADE 最成熟的机制解释，即与病原体结合的交叉反应性疾病增强抗体与 Fc 受体相互作用，从而增强病原体的进入或复制，最终增加病原体的总负荷。此外，我们还探讨了一些致病性抗体是如何使细菌免于补体依赖性杀灭，从而提高细菌存活率的。我们探究了抗体在没有增加病原体复制的情况下扩大炎症以导致严重疾病的分子机制。我们还研究了自身抗体在增强传染病发病机制方面的新作用。最后，我们将讨论如何利用这些见解来改进疫苗设计和未来的传染病治疗方法。
{"title":"Mechanisms of antibody-dependent enhancement of infectious disease","authors":"Timothy J. Wells, Tyron Esposito, Ian R. Henderson, Larisa I. Labzin","doi":"10.1038/s41577-024-01067-9","DOIUrl":"10.1038/s41577-024-01067-9","url":null,"abstract":"Antibody-dependent enhancement (ADE) of infectious disease is a phenomenon whereby host antibodies increase the severity of an infection. It is well established in viral infections but ADE also has an underappreciated role during bacterial, fungal and parasitic infections. ADE can occur during both primary infections and re-infections with the same or a related pathogen; therefore, understanding the underlying mechanisms of ADE is critical for understanding the pathogenesis and progression of many infectious diseases. Here, we review the four distinct mechanisms by which antibodies increase disease severity during an infection. We discuss the most established mechanistic explanation for ADE, where cross-reactive, disease-enhancing antibodies bound to pathogens interact with Fc receptors, thereby enhancing pathogen entry or replication, ultimately increasing the total pathogen load. Additionally, we explore how some pathogenic antibodies can shield bacteria from complement-dependent killing, thereby enhancing bacterial survival. We interrogate the molecular mechanisms by which antibodies can amplify inflammation to drive severe disease, even in the absence of increased pathogen replication. We also examine emerging roles for autoantibodies in enhancing the pathogenesis of infectious diseases. Finally, we discuss how we can leverage these insights to improve vaccine design and future treatments for infectious diseases. This Review discusses the different mechanisms of antibody-dependent enhancement (ADE) of infectious disease, including how antibodies can increase the pathogen load, protect bacteria from the immune system and amplify inflammation. The authors also highlight the role of autoantibodies and consider how a better understanding of ADE can be used to improve vaccines and treatments for infectious diseases.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141908901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Non-classical monocytes have the support of the whole vascular tree","authors":"Kirsty Minton","doi":"10.1038/s41577-024-01078-6","DOIUrl":"10.1038/s41577-024-01078-6","url":null,"abstract":"Thierry, Baudon et al. show that non-classical monocytes are nurtured by endothelial cell expression of CSF1 throughout the whole vascular tree.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141904614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-29DOI: 10.1038/s41577-024-01074-w
Alexandra Flemming
Neuroinflammation in response to infection or chronic disease can cause non-neural symptoms such as fatigue and muscle pain. Yang et al. show that CNS-derived IL-6 directly regulates muscle physiology.
{"title":"How neuroinflammation weakens muscles","authors":"Alexandra Flemming","doi":"10.1038/s41577-024-01074-w","DOIUrl":"10.1038/s41577-024-01074-w","url":null,"abstract":"Neuroinflammation in response to infection or chronic disease can cause non-neural symptoms such as fatigue and muscle pain. Yang et al. show that CNS-derived IL-6 directly regulates muscle physiology.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141790928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-29DOI: 10.1038/s41577-024-01072-y
Lucy Bird
Transient depletion of the gut microbiome by antibiotics in early life reduces systemic levels of the metabolite indole-3-propionic acid, which causes long-lasting mitochondrial damage to lung epithelial cells and increases susceptibility to airway inflammation in adult mice.
{"title":"Early life antibiotics have lasting effects on the lung epithelium","authors":"Lucy Bird","doi":"10.1038/s41577-024-01072-y","DOIUrl":"10.1038/s41577-024-01072-y","url":null,"abstract":"Transient depletion of the gut microbiome by antibiotics in early life reduces systemic levels of the metabolite indole-3-propionic acid, which causes long-lasting mitochondrial damage to lung epithelial cells and increases susceptibility to airway inflammation in adult mice.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141790929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-29DOI: 10.1038/s41577-024-01069-7
Qirong Lin, Kim Thrane, Camilla Engblom
In this Tools of the Trade article, Camilla Engblom and colleagues describe their elegant technique ‘Spatial VDJ’ to detect and map antigen receptor sequences in human tissue sections.
{"title":"Location matters: mapping antigen receptors within tissues","authors":"Qirong Lin, Kim Thrane, Camilla Engblom","doi":"10.1038/s41577-024-01069-7","DOIUrl":"10.1038/s41577-024-01069-7","url":null,"abstract":"In this Tools of the Trade article, Camilla Engblom and colleagues describe their elegant technique ‘Spatial VDJ’ to detect and map antigen receptor sequences in human tissue sections.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141791028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-25DOI: 10.1038/s41577-024-01061-1
Michael T. Lotze, Scott H. Olejniczak, Dimitris Skokos
Substantial progress in understanding T cell signalling, particularly with respect to T cell co-receptors such as the co-stimulatory receptor CD28, has been made in recent years. This knowledge has been instrumental in the development of innovative immunotherapies for patients with cancer, including immune checkpoint blockade antibodies, adoptive cell therapies, tumour-targeted immunostimulatory antibodies, and immunostimulatory small-molecule drugs that regulate T cell activation. Following the failed clinical trial of a CD28 superagonist antibody in 2006, targeted CD28 agonism has re-emerged as a technologically viable and clinically promising strategy for cancer immunotherapy. In this Review, we explore recent insights into the molecular functions and regulation of CD28. We describe how CD28 is central to the success of current cancer immunotherapies and examine how new questions arising from studies of CD28 as a clinical target have enhanced our understanding of its biological role and may guide the development of future therapeutic strategies in oncology. This Review covers recent advances in our understanding of CD28 co-stimulation of T cells and discusses an emerging paradigm that positions CD28 as central to the success of current and future immunotherapeutic approaches to treating cancer.
近年来，人们在了解 T 细胞信号，特别是 T 细胞共受体（如共刺激受体 CD28）方面取得了重大进展。这些知识有助于为癌症患者开发创新的免疫疗法，包括免疫检查点阻断抗体、收养细胞疗法、肿瘤靶向免疫刺激抗体和调节 T 细胞活化的免疫刺激小分子药物。继2006年CD28超拮抗剂抗体的临床试验失败后，靶向CD28激动剂作为一种技术上可行、临床上有前景的癌症免疫疗法策略重新崛起。在本综述中，我们将探讨 CD28 分子功能和调控的最新研究成果。我们描述了 CD28 如何成为当前癌症免疫疗法成功的核心，并探讨了将 CD28 作为临床靶点的研究中出现的新问题如何增进了我们对其生物学作用的了解，以及如何指导未来肿瘤学治疗策略的开发。
{"title":"CD28 co-stimulation: novel insights and applications in cancer immunotherapy","authors":"Michael T. Lotze, Scott H. Olejniczak, Dimitris Skokos","doi":"10.1038/s41577-024-01061-1","DOIUrl":"10.1038/s41577-024-01061-1","url":null,"abstract":"Substantial progress in understanding T cell signalling, particularly with respect to T cell co-receptors such as the co-stimulatory receptor CD28, has been made in recent years. This knowledge has been instrumental in the development of innovative immunotherapies for patients with cancer, including immune checkpoint blockade antibodies, adoptive cell therapies, tumour-targeted immunostimulatory antibodies, and immunostimulatory small-molecule drugs that regulate T cell activation. Following the failed clinical trial of a CD28 superagonist antibody in 2006, targeted CD28 agonism has re-emerged as a technologically viable and clinically promising strategy for cancer immunotherapy. In this Review, we explore recent insights into the molecular functions and regulation of CD28. We describe how CD28 is central to the success of current cancer immunotherapies and examine how new questions arising from studies of CD28 as a clinical target have enhanced our understanding of its biological role and may guide the development of future therapeutic strategies in oncology. This Review covers recent advances in our understanding of CD28 co-stimulation of T cells and discusses an emerging paradigm that positions CD28 as central to the success of current and future immunotherapeutic approaches to treating cancer.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":null,"pages":null},"PeriodicalIF":67.7,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141759985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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