Pub Date : 2024-11-26DOI: 10.1038/s41577-024-01116-3
Zi Yan Chen, Arthur Mortha
A preprint by Villar-Vesga et al. shows that monocyte-derived cells in the central nervous system produce mitochondrial reactive oxygen species to promote neuroinflammation.
{"title":"Mitochondria in monocyte-derived cells promote tissue damage in multiple sclerosis","authors":"Zi Yan Chen, Arthur Mortha","doi":"10.1038/s41577-024-01116-3","DOIUrl":"10.1038/s41577-024-01116-3","url":null,"abstract":"A preprint by Villar-Vesga et al. shows that monocyte-derived cells in the central nervous system produce mitochondrial reactive oxygen species to promote neuroinflammation.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"3-3"},"PeriodicalIF":67.7,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142712525","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 : 2024-11-25DOI: 10.1038/s41577-024-01117-2
Matthew Jackson, Eileen E. Parkes
A preprint by Hor et al. shows that PD1 signalling regulates the maintenance of a high-affinity, stem-like T cell subset in tumour-draining lymph nodes.
Hor等人的预印本显示，PD1信号调节着肿瘤引流淋巴结中高亲和性干样T细胞亚群的维持。
{"title":"Redefining PD1 as a guardian of stem-like T cells","authors":"Matthew Jackson, Eileen E. Parkes","doi":"10.1038/s41577-024-01117-2","DOIUrl":"10.1038/s41577-024-01117-2","url":null,"abstract":"A preprint by Hor et al. shows that PD1 signalling regulates the maintenance of a high-affinity, stem-like T cell subset in tumour-draining lymph nodes.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"3-3"},"PeriodicalIF":67.7,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696628","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 : 2024-11-19DOI: 10.1038/s41577-024-01108-3
Barbara Rehermann, Andrea L. Graham, David Masopust, Sara E. Hamilton
Fundamental discoveries in many aspects of mammalian physiology have been made using laboratory mice as research models. These studies have been facilitated by the genetic tractability and inbreeding of such mice, the large set of immunological reagents that are available, and the establishment of environmentally controlled, high-throughput facilities. Such facilities typically include barriers to keep the mouse colonies free of pathogens and the frequent re-derivation of the mice severely limits their commensal flora. Because humans have co-evolved with microorganisms and are exposed to a variety of pathogens, a growing community of researchers posits that preclinical disease research can be improved by studying mice in the context of the microbiota and pathogens that they would encounter in the natural world. Here, we provide a perspective of how these different approaches can be combined and integrated to improve existing mouse models to enhance our understanding of disease mechanisms and develop new therapies for humans. We also propose that the term ‘mice with natural microbiota’ is more appropriate for describing these models than existing terms such as ‘dirty mice’. There is emerging evidence that mice with a history of microbial exposures can better model the human immune system than laboratory mice maintained in pathogen-free conditions. In this Perspective, Rehermann and colleagues summarize different approaches that have been used to incorporate microbiota and pathogen exposures into laboratory mouse models. They suggest that the term ‘mice with natural microbiota’ should be used instead of ‘dirty mice’ to describe these systems in the future.
{"title":"Integrating natural commensals and pathogens into preclinical mouse models","authors":"Barbara Rehermann, Andrea L. Graham, David Masopust, Sara E. Hamilton","doi":"10.1038/s41577-024-01108-3","DOIUrl":"10.1038/s41577-024-01108-3","url":null,"abstract":"Fundamental discoveries in many aspects of mammalian physiology have been made using laboratory mice as research models. These studies have been facilitated by the genetic tractability and inbreeding of such mice, the large set of immunological reagents that are available, and the establishment of environmentally controlled, high-throughput facilities. Such facilities typically include barriers to keep the mouse colonies free of pathogens and the frequent re-derivation of the mice severely limits their commensal flora. Because humans have co-evolved with microorganisms and are exposed to a variety of pathogens, a growing community of researchers posits that preclinical disease research can be improved by studying mice in the context of the microbiota and pathogens that they would encounter in the natural world. Here, we provide a perspective of how these different approaches can be combined and integrated to improve existing mouse models to enhance our understanding of disease mechanisms and develop new therapies for humans. We also propose that the term ‘mice with natural microbiota’ is more appropriate for describing these models than existing terms such as ‘dirty mice’. There is emerging evidence that mice with a history of microbial exposures can better model the human immune system than laboratory mice maintained in pathogen-free conditions. In this Perspective, Rehermann and colleagues summarize different approaches that have been used to incorporate microbiota and pathogen exposures into laboratory mouse models. They suggest that the term ‘mice with natural microbiota’ should be used instead of ‘dirty mice’ to describe these systems in the future.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"1-13"},"PeriodicalIF":67.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142670686","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 : 2024-11-19DOI: 10.1038/s41577-024-01113-6
Katherine Whalley
ILC2s promote inhibitory synapse formation in the postnatal mouse brain through the production of IL-13.
ILC2 通过产生 IL-13 促进出生后小鼠大脑抑制性突触的形成。
{"title":"Innate lymphoid cell control of neuronal synapse development","authors":"Katherine Whalley","doi":"10.1038/s41577-024-01113-6","DOIUrl":"10.1038/s41577-024-01113-6","url":null,"abstract":"ILC2s promote inhibitory synapse formation in the postnatal mouse brain through the production of IL-13.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 1","pages":"2-2"},"PeriodicalIF":67.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142670683","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 : 2024-11-12DOI: 10.1038/s41577-024-01100-x
Heather D. Hickman, Niki M. Moutsopoulos
Individual tissues have distinct antiviral properties garnered through various mechanisms, including physical characteristics, tissue-resident immune cells and commensal organisms. Although the oral mucosa has long been appreciated as a critical barrier tissue that is exposed to a continuous barrage of pathogens, many fundamental aspects of the antiviral immune response in this tissue remain unknown. Several viral pathogens, such as herpesviruses and human papillomaviruses, have been acknowledged both historically and at present for infections in the oral cavity that result in substantial clinical burden. However, recent viral outbreaks, including those with SARS-CoV-2 and mpox, featured oral symptoms even though these viruses are not generally considered oral pathogens. Ensuing studies have shown that the oral cavity is an important locale for viral infection and potential transmission of newly emergent or re-emergent pathogens, highlighting the need for an increased understanding of the mechanisms of antiviral immunity at this site. In this Review, we provide a broad overview of antiviral immune responses in the oral cavity and discuss common viral infections and their manifestations in the oral mucosa. In addition, we present current mouse models for the study of oral viral infections. The oral mucosa is a critical barrier tissue that is continually exposed to pathogens, but antiviral immune responses in this tissue are poorly understood. Moreover, recent viral outbreaks, including SARS-CoV-2 and mpox, feature oral symptoms. This Review discusses antiviral immunity in the oral cavity and presents current mouse models for the study of oral viral infections.
{"title":"Viral infection and antiviral immunity in the oral cavity","authors":"Heather D. Hickman, Niki M. Moutsopoulos","doi":"10.1038/s41577-024-01100-x","DOIUrl":"10.1038/s41577-024-01100-x","url":null,"abstract":"Individual tissues have distinct antiviral properties garnered through various mechanisms, including physical characteristics, tissue-resident immune cells and commensal organisms. Although the oral mucosa has long been appreciated as a critical barrier tissue that is exposed to a continuous barrage of pathogens, many fundamental aspects of the antiviral immune response in this tissue remain unknown. Several viral pathogens, such as herpesviruses and human papillomaviruses, have been acknowledged both historically and at present for infections in the oral cavity that result in substantial clinical burden. However, recent viral outbreaks, including those with SARS-CoV-2 and mpox, featured oral symptoms even though these viruses are not generally considered oral pathogens. Ensuing studies have shown that the oral cavity is an important locale for viral infection and potential transmission of newly emergent or re-emergent pathogens, highlighting the need for an increased understanding of the mechanisms of antiviral immunity at this site. In this Review, we provide a broad overview of antiviral immune responses in the oral cavity and discuss common viral infections and their manifestations in the oral mucosa. In addition, we present current mouse models for the study of oral viral infections. The oral mucosa is a critical barrier tissue that is continually exposed to pathogens, but antiviral immune responses in this tissue are poorly understood. Moreover, recent viral outbreaks, including SARS-CoV-2 and mpox, feature oral symptoms. This Review discusses antiviral immunity in the oral cavity and presents current mouse models for the study of oral viral infections.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"1-15"},"PeriodicalIF":67.7,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142599167","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 : 2024-11-11DOI: 10.1038/s41577-024-01105-6
Xiaoshan Shi, Xing He, Chenqi Xu
Immunoreceptors have crucial roles in sensing environmental signals and initiating immune responses to protect the host. Dysregulation of immunoreceptor signalling can therefore lead to a range of diseases, making immunoreceptor-based therapies a promising frontier in biomedicine. A common feature of various immunoreceptors is the basic-residue-rich sequence (BRS), which is a largely unexplored aspect of immunoreceptor signalling. The BRS is typically located in the cytoplasmic juxtamembrane region of immunoreceptors, where it forms dynamic interactions with neighbouring charged molecules to regulate signalling. Loss or gain of the basic residues in an immunoreceptor BRS has been linked to severe human diseases, such as immunodeficiency and autoimmunity. In this Perspective, we describe the role of BRSs in various immunoreceptors, elucidating their signalling mechanisms and biological functions. Furthermore, we highlight pathogenic mutations in immunoreceptor BRSs and discuss the potential of leveraging BRS signalling in engineered T cell-based therapies. The basic-residue-rich sequence (BRS) is a common motif located in the cytoplasmic tail of most immunoreceptors. This Perspective highlights the mechanisms of BRS signalling, its pathophysiological importance and how to harness BRS signalling to develop next-generation immunotherapy.
{"title":"Charge-based immunoreceptor signalling in health and disease","authors":"Xiaoshan Shi, Xing He, Chenqi Xu","doi":"10.1038/s41577-024-01105-6","DOIUrl":"10.1038/s41577-024-01105-6","url":null,"abstract":"Immunoreceptors have crucial roles in sensing environmental signals and initiating immune responses to protect the host. Dysregulation of immunoreceptor signalling can therefore lead to a range of diseases, making immunoreceptor-based therapies a promising frontier in biomedicine. A common feature of various immunoreceptors is the basic-residue-rich sequence (BRS), which is a largely unexplored aspect of immunoreceptor signalling. The BRS is typically located in the cytoplasmic juxtamembrane region of immunoreceptors, where it forms dynamic interactions with neighbouring charged molecules to regulate signalling. Loss or gain of the basic residues in an immunoreceptor BRS has been linked to severe human diseases, such as immunodeficiency and autoimmunity. In this Perspective, we describe the role of BRSs in various immunoreceptors, elucidating their signalling mechanisms and biological functions. Furthermore, we highlight pathogenic mutations in immunoreceptor BRSs and discuss the potential of leveraging BRS signalling in engineered T cell-based therapies. The basic-residue-rich sequence (BRS) is a common motif located in the cytoplasmic tail of most immunoreceptors. This Perspective highlights the mechanisms of BRS signalling, its pathophysiological importance and how to harness BRS signalling to develop next-generation immunotherapy.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"1-14"},"PeriodicalIF":67.7,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142599168","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 : 2024-11-07DOI: 10.1038/s41577-024-01102-9
Guido Kroemer, Léa Montégut, Oliver Kepp, Laurence Zitvogel
The danger theory of immunity, introduced by Polly Matzinger in 1994, posits that tissue stress, damage or infection has a decisive role in determining immune responses. Since then, a growing body of evidence has supported the idea that the capacity to elicit cognate immune responses (immunogenicity) relies on the combination of antigenicity (the ability to be recognized by T cell receptors or antibodies) and adjuvanticity (additional signals arising owing to tissue damage). Here, we discuss the molecular foundations of the danger theory while focusing on immunologically relevant damage-associated molecular patterns, microorganism-associated molecular patterns, and neuroendocrine stress-associated immunomodulatory molecules, as well as on their receptors. We critically evaluate patient-relevant evidence, examining how cancer cells and pathogenic viruses suppress damage-associated molecular patterns to evade immune recognition, how intestinal dysbiosis can reduce immunostimulatory microorganism-associated molecular patterns and compromise immune responses, and which hereditary immune defects support the validity of the danger theory. Furthermore, we incorporate the danger hypothesis into a close-to-fail-safe hierarchy of immunological tolerance mechanisms that also involve the clonal deletion and inactivation of immune cells. Thirty years ago, Polly Matzinger introduced the ‘danger theory of immunity’, which proposed that danger and damage have a decisive role in immune responses. In this Perspective, Kroemer et al. reflect on the impact of the danger theory, discuss its molecular foundations and present an extended version of it. They propose that immunological self-tolerance is organized in a hierarchy that functions in a close-to-fail-safe cascade-like fashion, thereby reconciling Matzinger’s danger theory with the self–non-self-discrimination hypothesis.
波莉-马津格（Polly Matzinger）于 1994 年提出的免疫危险理论认为，组织应激、损伤或感染在决定免疫反应方面起着决定性作用。从那时起，越来越多的证据支持这一观点，即引起同种免疫反应的能力（免疫原性）依赖于抗原性（被 T 细胞受体或抗体识别的能力）和佐剂性（由于组织损伤而产生的额外信号）的结合。在此，我们将讨论危险理论的分子基础，同时重点关注与免疫相关的损伤相关分子模式、微生物相关分子模式、神经内分泌应激相关免疫调节分子及其受体。我们严格评估与患者相关的证据，研究癌细胞和致病病毒如何抑制损伤相关分子模式以逃避免疫识别，肠道菌群失调如何减少免疫刺激微生物相关分子模式并损害免疫反应，以及哪些遗传性免疫缺陷支持危险理论的有效性。此外，我们还将危险假说纳入了免疫耐受机制的近乎安全的层次结构中，其中也涉及免疫细胞的克隆性删除和失活。
{"title":"The danger theory of immunity revisited","authors":"Guido Kroemer, Léa Montégut, Oliver Kepp, Laurence Zitvogel","doi":"10.1038/s41577-024-01102-9","DOIUrl":"10.1038/s41577-024-01102-9","url":null,"abstract":"The danger theory of immunity, introduced by Polly Matzinger in 1994, posits that tissue stress, damage or infection has a decisive role in determining immune responses. Since then, a growing body of evidence has supported the idea that the capacity to elicit cognate immune responses (immunogenicity) relies on the combination of antigenicity (the ability to be recognized by T cell receptors or antibodies) and adjuvanticity (additional signals arising owing to tissue damage). Here, we discuss the molecular foundations of the danger theory while focusing on immunologically relevant damage-associated molecular patterns, microorganism-associated molecular patterns, and neuroendocrine stress-associated immunomodulatory molecules, as well as on their receptors. We critically evaluate patient-relevant evidence, examining how cancer cells and pathogenic viruses suppress damage-associated molecular patterns to evade immune recognition, how intestinal dysbiosis can reduce immunostimulatory microorganism-associated molecular patterns and compromise immune responses, and which hereditary immune defects support the validity of the danger theory. Furthermore, we incorporate the danger hypothesis into a close-to-fail-safe hierarchy of immunological tolerance mechanisms that also involve the clonal deletion and inactivation of immune cells. Thirty years ago, Polly Matzinger introduced the ‘danger theory of immunity’, which proposed that danger and damage have a decisive role in immune responses. In this Perspective, Kroemer et al. reflect on the impact of the danger theory, discuss its molecular foundations and present an extended version of it. They propose that immunological self-tolerance is organized in a hierarchy that functions in a close-to-fail-safe cascade-like fashion, thereby reconciling Matzinger’s danger theory with the self–non-self-discrimination hypothesis.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"24 12","pages":"912-928"},"PeriodicalIF":67.7,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41577-024-01102-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142596852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-07DOI: 10.1038/s41577-024-01103-8
Herbert Tilg, Gianluca Ianiro, Antonio Gasbarrini, Timon E. Adolph
Adipose tissue is an immunologically active organ that controls host physiology, partly through the release of mediators termed adipokines. In obesity, adipocytes and infiltrating leukocytes produce adipokines, which include the hormones adiponectin and leptin and cytokines such as tumour necrosis factor and IL-1β. These adipokines orchestrate immune responses that are collectively referred to as metabolic inflammation. Consequently, metabolic inflammation characterizes metabolic disorders and promotes distinct disease aspects, such as insulin resistance, metabolic dysfunction-associated liver disease and cardiovascular complications. In this unifying concept, adipokines participate in the immunological cross-talk that occurs between metabolically active organs in metabolic diseases, highlighting the fundamental role of adipokines in obesity and their potential for therapeutic intervention. Here, we summarize how adipokines shape metabolic inflammation in mice and humans, focusing on their contribution to metabolic disorders in the setting of obesity and discussing their value as therapeutic targets. This Review discusses how adipose tissue can regulate host immune function via the release of adipokines, including adiponectin, leptin and various cytokines. These adipokines contribute to immune responses and metabolic inflammation and can have both beneficial and detrimental effects on host physiology. In obesity, adipokine release can promote insulin resistance and cardiovascular diseases; as such, there is interest in targeting these mediators for therapy of various metabolic disorders.
{"title":"Adipokines: masterminds of metabolic inflammation","authors":"Herbert Tilg, Gianluca Ianiro, Antonio Gasbarrini, Timon E. Adolph","doi":"10.1038/s41577-024-01103-8","DOIUrl":"10.1038/s41577-024-01103-8","url":null,"abstract":"Adipose tissue is an immunologically active organ that controls host physiology, partly through the release of mediators termed adipokines. In obesity, adipocytes and infiltrating leukocytes produce adipokines, which include the hormones adiponectin and leptin and cytokines such as tumour necrosis factor and IL-1β. These adipokines orchestrate immune responses that are collectively referred to as metabolic inflammation. Consequently, metabolic inflammation characterizes metabolic disorders and promotes distinct disease aspects, such as insulin resistance, metabolic dysfunction-associated liver disease and cardiovascular complications. In this unifying concept, adipokines participate in the immunological cross-talk that occurs between metabolically active organs in metabolic diseases, highlighting the fundamental role of adipokines in obesity and their potential for therapeutic intervention. Here, we summarize how adipokines shape metabolic inflammation in mice and humans, focusing on their contribution to metabolic disorders in the setting of obesity and discussing their value as therapeutic targets. This Review discusses how adipose tissue can regulate host immune function via the release of adipokines, including adiponectin, leptin and various cytokines. These adipokines contribute to immune responses and metabolic inflammation and can have both beneficial and detrimental effects on host physiology. In obesity, adipokine release can promote insulin resistance and cardiovascular diseases; as such, there is interest in targeting these mediators for therapy of various metabolic disorders.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"1-16"},"PeriodicalIF":67.7,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142594375","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 : 2024-10-31DOI: 10.1038/s41577-024-01099-1
Muzlifah Haniffa, Aidan Maartens, Elena Winheim, Laura Jardine
The human immune system is made up of a huge variety of cell types each with unique functions. Local networks of resident immune cells are poised to sense and protect against pathogen entry, whereas more widespread innate and adaptive immune networks provide first rapid, then long-lasting and targeted responses. However, how we develop such a diverse and complex system remains unknown. Studying human development directly has been challenging in the past, but recent advances in single-cell and spatial genomics, together with the co-ordinated efforts of the Human Cell Atlas and other initiatives, have led to new studies that map the development of the human immune system in unprecedented detail. In this Review, we consider the timings, transitions, cell types and tissue microenvironments that are crucial for building the human immune system. We also compare and contrast the human system with model species and in vitro systems, and discuss how an understanding of prenatal immune system development will improve our knowledge of human disease. Single-cell multi-omic profiling has revealed how the immune system is established in the human embryo, mapping in unprecedented detail the emergence of progenitors, the handover of haematopoiesis between sites and the diversification of cell lineages across the body.
{"title":"Decoding the human prenatal immune system with single-cell multi-omics","authors":"Muzlifah Haniffa, Aidan Maartens, Elena Winheim, Laura Jardine","doi":"10.1038/s41577-024-01099-1","DOIUrl":"10.1038/s41577-024-01099-1","url":null,"abstract":"The human immune system is made up of a huge variety of cell types each with unique functions. Local networks of resident immune cells are poised to sense and protect against pathogen entry, whereas more widespread innate and adaptive immune networks provide first rapid, then long-lasting and targeted responses. However, how we develop such a diverse and complex system remains unknown. Studying human development directly has been challenging in the past, but recent advances in single-cell and spatial genomics, together with the co-ordinated efforts of the Human Cell Atlas and other initiatives, have led to new studies that map the development of the human immune system in unprecedented detail. In this Review, we consider the timings, transitions, cell types and tissue microenvironments that are crucial for building the human immune system. We also compare and contrast the human system with model species and in vitro systems, and discuss how an understanding of prenatal immune system development will improve our knowledge of human disease. Single-cell multi-omic profiling has revealed how the immune system is established in the human embryo, mapping in unprecedented detail the emergence of progenitors, the handover of haematopoiesis between sites and the diversification of cell lineages across the body.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"1-13"},"PeriodicalIF":67.7,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142556341","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 : 2024-10-30DOI: 10.1038/s41577-024-01109-2
Alexandra Flemming
Inflammation and fibrosis are linked to organ dysfunction. Two studies in Nature investigate the cross-talk between immune cells and fibroblasts in the context of heart disease and identify potential targets for therapy.
{"title":"Insights into immune cell–fibroblast communication in heart disease","authors":"Alexandra Flemming","doi":"10.1038/s41577-024-01109-2","DOIUrl":"10.1038/s41577-024-01109-2","url":null,"abstract":"Inflammation and fibrosis are linked to organ dysfunction. Two studies in Nature investigate the cross-talk between immune cells and fibroblasts in the context of heart disease and identify potential targets for therapy.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"24 12","pages":"849-849"},"PeriodicalIF":67.7,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142541586","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：