Pub Date : 2025-09-01DOI: 10.1038/s41577-025-01224-8
Lucy Bird
B cells that expand following infection with EBV can colonize the brain, where they recruit activated T cells that have potential to cause neuronal damage, thereby providing a mechanism to explain the link between EBV and increased MS risk.
{"title":"B cell trailblazers connect EBV to MS","authors":"Lucy Bird","doi":"10.1038/s41577-025-01224-8","DOIUrl":"10.1038/s41577-025-01224-8","url":null,"abstract":"B cells that expand following infection with EBV can colonize the brain, where they recruit activated T cells that have potential to cause neuronal damage, thereby providing a mechanism to explain the link between EBV and increased MS risk.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 10","pages":"707-707"},"PeriodicalIF":60.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144924216","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 : 2025-09-01DOI: 10.1038/s41577-025-01225-7
Yvonne Bordon
Populations of regulatory KIR+CD8+ T cells expand during pregnancy and can promote maternal tolerance to the developing fetus.
调节性KIR+CD8+ T细胞群体在怀孕期间扩增，可以促进母体对发育中的胎儿的耐受性。
{"title":"Regulatory KIR+CD8+ T cells in pregnancy","authors":"Yvonne Bordon","doi":"10.1038/s41577-025-01225-7","DOIUrl":"10.1038/s41577-025-01225-7","url":null,"abstract":"Populations of regulatory KIR+CD8+ T cells expand during pregnancy and can promote maternal tolerance to the developing fetus.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 10","pages":"709-709"},"PeriodicalIF":60.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928011","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":"Clock genes keep intestinal ILC3s ticking","authors":"Kirsty Minton","doi":"10.1038/s41577-025-01220-y","DOIUrl":"10.1038/s41577-025-01220-y","url":null,"abstract":"A study by Bhattarai et al. in Nature Immunology reports that ILC3-to-ILC1 plasticity in the gut is regulated by circadian clock proteins.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 10","pages":"708-708"},"PeriodicalIF":60.9,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144915660","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 : 2025-08-14DOI: 10.1038/s41577-025-01211-z
Ashraf Ul Kabir, Madhav Subramanian, Yoojung Kwon, Kyunghee Choi
Immune checkpoint blockade therapy has revolutionized the treatment of metastatic and solid tumours, achieving durable responses in a subset of patients. However, most patients do not respond to immune checkpoint blockade, underscoring the critical need to better understand the determinants of therapeutic efficacy. A key obstacle to effective antitumour immune responses is the abnormal structure and function of tumour-associated blood vessels, which impede immune cell infiltration and contribute to the development of an immunosuppressive tumour microenvironment. Current research highlights the inverse correlation between angiogenesis and immune activity within the tumour microenvironment. In this Review, we discuss tumour angiogenesis in the context of tumour immunity, examining how this affects tumour progression and immunotherapy outcomes. We examine the molecular mechanisms underlying the crosstalk between angiogenesis and tumour immunity and discuss emerging anti-angiogenic regulators that hold potential for combination therapies. By integrating insights from preclinical and clinical studies, we outline future research directions to address current challenges and optimize cancer treatment strategies through combined anti-angiogenic and immunotherapeutic approaches. Tumour-associated blood vessels are abnormal in structure and function, and this can limit immune cell infiltration into tumours and contribute to the immunosuppressive tumour microenvironment. This Review highlights how tumour angiogenesis impacts antitumour immunity and explains why combining anti-angiogenic strategies with immunotherapies could improve clinical outcomes for patients with cancer.
{"title":"Linking tumour angiogenesis and tumour immunity","authors":"Ashraf Ul Kabir, Madhav Subramanian, Yoojung Kwon, Kyunghee Choi","doi":"10.1038/s41577-025-01211-z","DOIUrl":"10.1038/s41577-025-01211-z","url":null,"abstract":"Immune checkpoint blockade therapy has revolutionized the treatment of metastatic and solid tumours, achieving durable responses in a subset of patients. However, most patients do not respond to immune checkpoint blockade, underscoring the critical need to better understand the determinants of therapeutic efficacy. A key obstacle to effective antitumour immune responses is the abnormal structure and function of tumour-associated blood vessels, which impede immune cell infiltration and contribute to the development of an immunosuppressive tumour microenvironment. Current research highlights the inverse correlation between angiogenesis and immune activity within the tumour microenvironment. In this Review, we discuss tumour angiogenesis in the context of tumour immunity, examining how this affects tumour progression and immunotherapy outcomes. We examine the molecular mechanisms underlying the crosstalk between angiogenesis and tumour immunity and discuss emerging anti-angiogenic regulators that hold potential for combination therapies. By integrating insights from preclinical and clinical studies, we outline future research directions to address current challenges and optimize cancer treatment strategies through combined anti-angiogenic and immunotherapeutic approaches. Tumour-associated blood vessels are abnormal in structure and function, and this can limit immune cell infiltration into tumours and contribute to the immunosuppressive tumour microenvironment. This Review highlights how tumour angiogenesis impacts antitumour immunity and explains why combining anti-angiogenic strategies with immunotherapies could improve clinical outcomes for patients with cancer.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 1","pages":"35-51"},"PeriodicalIF":60.9,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144840128","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 : 2025-08-08DOI: 10.1038/s41577-025-01208-8
Florian Huber, Michal Bassani-Sternberg
Human tumour cells express mutated and non-mutated proteins that can be processed and presented by these cells as peptides bound to human leukocyte antigen (HLA). Some of these peptides are recognized by cognate T cell receptors as ‘non-self’, leading to specific killing of tumour cells by T cells. This process is fundamental to the success of cancer immunotherapy, which exploits the ability of the immune system to eliminate transformed cells. Mutated antigens (neoantigens) have been implicated in the remarkable therapeutic efficacy of immune checkpoint inhibitors (ICIs), which boost endogenous antitumour immune responses. In recent years, the combination of ICIs with personalized cancer vaccines that target neoantigens and other tumour-specific antigens has emerged as a new therapeutic strategy. However, the robust immune pressure that ICIs exert on cancer cells inevitably amplifies the phenomenon of immune editing, which can allow cancer cells to develop resistance mechanisms that subvert surveillance by the immune system. Diminished antigenicity can be due to defects in the antigen processing and presentation machinery, such as HLA-I/II loss of heterozygosity and loss of functional β2-microglobulin. This poses a considerable challenge for combination therapies that include ICIs and for the design of cancer-specific vaccines. Effective tumour-specific T cell immunity — and the success of cancer immunotherapies — relies on the presentation of antigens via human leukocyte antigen (HLA) molecules. In this Review, Bassani-Sternberg and Huber explore recent advances in understanding the repertoire of tumour-specific antigens, as well as how disruptions in antigen processing and presentation contribute to immune evasion and resistance to immune checkpoint blockade. The authors also highlight how these insights can inform the design of personalized neoantigen-based vaccines and combination therapies aimed at outpacing tumour immunoediting.
{"title":"Defects in antigen processing and presentation: mechanisms, immune evasion and implications for cancer vaccine development","authors":"Florian Huber, Michal Bassani-Sternberg","doi":"10.1038/s41577-025-01208-8","DOIUrl":"10.1038/s41577-025-01208-8","url":null,"abstract":"Human tumour cells express mutated and non-mutated proteins that can be processed and presented by these cells as peptides bound to human leukocyte antigen (HLA). Some of these peptides are recognized by cognate T cell receptors as ‘non-self’, leading to specific killing of tumour cells by T cells. This process is fundamental to the success of cancer immunotherapy, which exploits the ability of the immune system to eliminate transformed cells. Mutated antigens (neoantigens) have been implicated in the remarkable therapeutic efficacy of immune checkpoint inhibitors (ICIs), which boost endogenous antitumour immune responses. In recent years, the combination of ICIs with personalized cancer vaccines that target neoantigens and other tumour-specific antigens has emerged as a new therapeutic strategy. However, the robust immune pressure that ICIs exert on cancer cells inevitably amplifies the phenomenon of immune editing, which can allow cancer cells to develop resistance mechanisms that subvert surveillance by the immune system. Diminished antigenicity can be due to defects in the antigen processing and presentation machinery, such as HLA-I/II loss of heterozygosity and loss of functional β2-microglobulin. This poses a considerable challenge for combination therapies that include ICIs and for the design of cancer-specific vaccines. Effective tumour-specific T cell immunity — and the success of cancer immunotherapies — relies on the presentation of antigens via human leukocyte antigen (HLA) molecules. In this Review, Bassani-Sternberg and Huber explore recent advances in understanding the repertoire of tumour-specific antigens, as well as how disruptions in antigen processing and presentation contribute to immune evasion and resistance to immune checkpoint blockade. The authors also highlight how these insights can inform the design of personalized neoantigen-based vaccines and combination therapies aimed at outpacing tumour immunoediting.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 1","pages":"23-34"},"PeriodicalIF":60.9,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144797256","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 : 2025-08-07DOI: 10.1038/s41577-025-01207-9
Andrew C. Chan, Greg D. Martyn, Paul J. Carter
In 1975, Köhler and Milstein invented hybridoma technology for the generation of murine monoclonal antibodies with predetermined antigen-binding specificity. The transformative impact of monoclonal antibodies is demonstrated by their ubiquitous use as biomedical research reagents and the worldwide approval of at least 212 antibody therapeutics with tens of millions of patients treated to date. Advances in antibody technologies, such as humanization and robust methods for human antibody generation, mitigated the major limitations of murine antibodies as therapeutics. These technologies, combined with progress in biomanufacturing, helped to launch this modern era of antibody therapeutics. Beyond IgG, antibody therapeutics have blossomed into multiple alternative formats, including bispecific antibodies and antibody–drug conjugates. Additionally, antibody fragments have been developed as stand-alone therapeutics and to target cell therapies, notably chimeric antigen receptor T cells. These advances in antibody technologies, plus innovation enabling subcutaneous delivery, have improved the therapeutic benefits and convenience of antibody treatment for many patients. This concept is illustrated here by multiple generations of antibody therapeutics for human epidermal growth factor receptor 2 (HER2)+ cancers and B cell-targeted therapies for haematological cancers and immunological diseases. Finally, we opine briefly on some of the many promising future directions with antibody therapeutics, including the application of artificial intelligence for antibody identification and multi-parameter optimization. Fifty years ago, Köhler and Milstein introduced the world to hybridoma technology for the generation of monoclonal antibodies. Scientists have subsequently built upon this seminal discovery to develop antibody-based therapies for numerous diseases, with millions of patients benefiting from such drugs. To mark 50 years of monoclonal antibodies, this Review from Chan, Martyn and Carter provides an overview of how antibody engineering strategies have continued to improve antibody-based therapeutics, chiefly focusing on antibody-mediated targeting of B cells and also human epidermal growth factor receptor 2 (HER2)+ cancers. The authors also highlight the promise of emerging tools, including artificial intelligence, for development of the next generation of antibody-based therapeutics.
{"title":"Fifty years of monoclonals: the past, present and future of antibody therapeutics","authors":"Andrew C. Chan, Greg D. Martyn, Paul J. Carter","doi":"10.1038/s41577-025-01207-9","DOIUrl":"10.1038/s41577-025-01207-9","url":null,"abstract":"In 1975, Köhler and Milstein invented hybridoma technology for the generation of murine monoclonal antibodies with predetermined antigen-binding specificity. The transformative impact of monoclonal antibodies is demonstrated by their ubiquitous use as biomedical research reagents and the worldwide approval of at least 212 antibody therapeutics with tens of millions of patients treated to date. Advances in antibody technologies, such as humanization and robust methods for human antibody generation, mitigated the major limitations of murine antibodies as therapeutics. These technologies, combined with progress in biomanufacturing, helped to launch this modern era of antibody therapeutics. Beyond IgG, antibody therapeutics have blossomed into multiple alternative formats, including bispecific antibodies and antibody–drug conjugates. Additionally, antibody fragments have been developed as stand-alone therapeutics and to target cell therapies, notably chimeric antigen receptor T cells. These advances in antibody technologies, plus innovation enabling subcutaneous delivery, have improved the therapeutic benefits and convenience of antibody treatment for many patients. This concept is illustrated here by multiple generations of antibody therapeutics for human epidermal growth factor receptor 2 (HER2)+ cancers and B cell-targeted therapies for haematological cancers and immunological diseases. Finally, we opine briefly on some of the many promising future directions with antibody therapeutics, including the application of artificial intelligence for antibody identification and multi-parameter optimization. Fifty years ago, Köhler and Milstein introduced the world to hybridoma technology for the generation of monoclonal antibodies. Scientists have subsequently built upon this seminal discovery to develop antibody-based therapies for numerous diseases, with millions of patients benefiting from such drugs. To mark 50 years of monoclonal antibodies, this Review from Chan, Martyn and Carter provides an overview of how antibody engineering strategies have continued to improve antibody-based therapeutics, chiefly focusing on antibody-mediated targeting of B cells and also human epidermal growth factor receptor 2 (HER2)+ cancers. The authors also highlight the promise of emerging tools, including artificial intelligence, for development of the next generation of antibody-based therapeutics.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 10","pages":"745-765"},"PeriodicalIF":60.9,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144792354","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 : 2025-07-29DOI: 10.1038/s41577-025-01206-w
Dina Hochhauser, Rotem Sorek
The cell-autonomous innate immune system is responsible for sensing and mitigating viral infection at the level of individual cells. Many of the mechanisms used by the cell-autonomous innate immune system in eukaryotic cells are ancient and have evolutionary roots in bacterial systems that defend against phage infection. Studies from recent years have shown that modification of the free nucleotide pool is central to many of these conserved immune mechanisms. In this Review, we explain how immune pathways manipulate the available pool of nucleotides to deprive viruses of molecules essential for their replication, how immune proteins chemically modify nucleotides to generate immune signalling molecules, and how cell-autonomous innate immune mechanisms produce altered nucleotides that poison viral replication. We also discuss the mechanisms used by viruses to antagonize nucleotide-based immunity. Finally, we explore the evolutionary logic of using nucleotides as building blocks for immune responses. Modification of the nucleotide pool is emerging as key to innate immunity in animals, plants and bacteria. This Review explains how immune pathways conserved from bacteria to humans manipulate the nucleotide pool to block viral replication and produce immune signalling molecules.
{"title":"Manipulation of the nucleotide pool in human, bacterial and plant immunity","authors":"Dina Hochhauser, Rotem Sorek","doi":"10.1038/s41577-025-01206-w","DOIUrl":"10.1038/s41577-025-01206-w","url":null,"abstract":"The cell-autonomous innate immune system is responsible for sensing and mitigating viral infection at the level of individual cells. Many of the mechanisms used by the cell-autonomous innate immune system in eukaryotic cells are ancient and have evolutionary roots in bacterial systems that defend against phage infection. Studies from recent years have shown that modification of the free nucleotide pool is central to many of these conserved immune mechanisms. In this Review, we explain how immune pathways manipulate the available pool of nucleotides to deprive viruses of molecules essential for their replication, how immune proteins chemically modify nucleotides to generate immune signalling molecules, and how cell-autonomous innate immune mechanisms produce altered nucleotides that poison viral replication. We also discuss the mechanisms used by viruses to antagonize nucleotide-based immunity. Finally, we explore the evolutionary logic of using nucleotides as building blocks for immune responses. Modification of the nucleotide pool is emerging as key to innate immunity in animals, plants and bacteria. This Review explains how immune pathways conserved from bacteria to humans manipulate the nucleotide pool to block viral replication and produce immune signalling molecules.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"26 1","pages":"7-22"},"PeriodicalIF":60.9,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719705","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 : 2025-07-28DOI: 10.1038/s41577-025-01217-7
Yvonne Bordon
Exercise promotes changes in the gut microbiota that enhance anti-tumour T cell responses.
运动促进肠道微生物群的变化，增强抗肿瘤T细胞反应。
{"title":"Exercise induces metabolic changes in the gut microbiota that enhance anti-tumour T cell responses","authors":"Yvonne Bordon","doi":"10.1038/s41577-025-01217-7","DOIUrl":"10.1038/s41577-025-01217-7","url":null,"abstract":"Exercise promotes changes in the gut microbiota that enhance anti-tumour T cell responses.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 9","pages":"634-634"},"PeriodicalIF":60.9,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144715334","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 : 2025-07-24DOI: 10.1038/s41577-025-01203-z
Enzo Z. Poirier
Stem cells maintain tissue architecture by replacing differentiated cells at steady state and upon injury. Implementing this cornerstone role requires protection of stem cells from pathogens and from the toxic effects of immune system activation. However, the pro-inflammatory innate immune mechanisms that protect differentiated cells from infection are poorly functional in stem cells. Instead, stem cells employ other specific defence mechanisms, such as antiviral RNA interference. At steady state, the proliferation and differentiation of tissue stem cells is regulated by multiple cell types, including immune cells. Following sterile tissue injury or during infection, the immune response — in addition to controlling pathogens and clearing cell debris — orchestrates tissue repair by fine-tuning stem cell activity, through direct cell–cell contacts and via inflammatory mediators such as cytokines. There is thus stem–immune cross-talk that is fundamental to the maintenance of tissue homeostasis. Inflammageing, which is defined as the age-driven elevation of inflammation and is associated with an altered immune cell composition, profoundly affects this stem–immune cross-talk, impacting the ability to repair tissues and participating in ageing of the whole organism. This Review by Poirier highlights the intrinsic mechanisms that protect stem cells from infection. The author also explains how stem cell populations in different tissue sites respond to infection or injury to protect tissue integrity, and the impact of inflammageing on these processes.
{"title":"How stem cells respond to infection, inflammation and ageing","authors":"Enzo Z. Poirier","doi":"10.1038/s41577-025-01203-z","DOIUrl":"10.1038/s41577-025-01203-z","url":null,"abstract":"Stem cells maintain tissue architecture by replacing differentiated cells at steady state and upon injury. Implementing this cornerstone role requires protection of stem cells from pathogens and from the toxic effects of immune system activation. However, the pro-inflammatory innate immune mechanisms that protect differentiated cells from infection are poorly functional in stem cells. Instead, stem cells employ other specific defence mechanisms, such as antiviral RNA interference. At steady state, the proliferation and differentiation of tissue stem cells is regulated by multiple cell types, including immune cells. Following sterile tissue injury or during infection, the immune response — in addition to controlling pathogens and clearing cell debris — orchestrates tissue repair by fine-tuning stem cell activity, through direct cell–cell contacts and via inflammatory mediators such as cytokines. There is thus stem–immune cross-talk that is fundamental to the maintenance of tissue homeostasis. Inflammageing, which is defined as the age-driven elevation of inflammation and is associated with an altered immune cell composition, profoundly affects this stem–immune cross-talk, impacting the ability to repair tissues and participating in ageing of the whole organism. This Review by Poirier highlights the intrinsic mechanisms that protect stem cells from infection. The author also explains how stem cell populations in different tissue sites respond to infection or injury to protect tissue integrity, and the impact of inflammageing on these processes.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 12","pages":"900-911"},"PeriodicalIF":60.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701339","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 : 2025-07-24DOI: 10.1038/s41577-025-01212-y
Qisi Zhang, Longlong Si
In this Tools of the Trade article, Qisi Zhang and Longlong Si describe a method for generating live attenuated vaccines that involves targeting viruses to the host cells’ protein degradation machinery, which attenuates the virus within the host and also enhances viral antigen presentation.
{"title":"Live vaccine development through targeted protein degradation","authors":"Qisi Zhang, Longlong Si","doi":"10.1038/s41577-025-01212-y","DOIUrl":"10.1038/s41577-025-01212-y","url":null,"abstract":"In this Tools of the Trade article, Qisi Zhang and Longlong Si describe a method for generating live attenuated vaccines that involves targeting viruses to the host cells’ protein degradation machinery, which attenuates the virus within the host and also enhances viral antigen presentation.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":"25 9","pages":"633-633"},"PeriodicalIF":60.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701340","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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