Pub Date : 2024-04-03DOI: 10.1038/s41577-024-01016-6
Daniel J. Rawle, Leon E. Hugo, Abigail L. Cox, Gregor J. Devine, Andreas Suhrbier
The World Health Organization recently declared a global initiative to control arboviral diseases. These are mainly caused by pathogenic flaviviruses (such as dengue, yellow fever and Zika viruses) and alphaviruses (such as chikungunya and Venezuelan equine encephalitis viruses). Vaccines represent key interventions for these viruses, with licensed human and/or veterinary vaccines being available for several members of both genera. However, a hurdle for the licensing of new vaccines is the epidemic nature of many arboviruses, which presents logistical challenges for phase III efficacy trials. Furthermore, our ability to predict or measure the post-vaccination immune responses that are sufficient for subclinical outcomes post-infection is limited. Given that arboviruses are also subject to control by the immune system of their insect vectors, several approaches are now emerging that aim to augment antiviral immunity in mosquitoes, including Wolbachia infection, transgenic mosquitoes, insect-specific viruses and paratransgenesis. In this Review, we discuss recent advances, current challenges and future prospects in exploiting both vertebrate and invertebrate immune systems for the control of flaviviral and alphaviral diseases. In this Review, the authors discuss recent advances, current challenges and future prospects in exploiting both vertebrate and invertebrate immune systems for the control of flaviviral and alphaviral diseases.
世界卫生组织最近宣布了一项控制虫媒病毒疾病的全球倡议。这些疾病主要由致病性黄病毒（如登革热、黄热病和寨卡病毒）和阿尔巴病毒（如基孔肯雅病毒和委内瑞拉马脑炎病毒）引起。疫苗是这些病毒的关键干预措施，目前已有针对这两个病毒属中若干成员的人类和/或兽医许可疫苗。然而，许多虫媒病毒具有流行性，这给 III 期药效试验带来了后勤方面的挑战，这也是新疫苗获得许可的一个障碍。此外，我们预测或测量疫苗接种后免疫反应的能力有限，而这种免疫反应足以在感染后产生亚临床结果。鉴于虫媒病毒也受其昆虫载体免疫系统的控制，目前出现了几种旨在增强蚊子抗病毒免疫力的方法，包括沃尔巴克氏体感染、转基因蚊子、昆虫特异性病毒和副转基因。在本综述中，我们将讨论利用脊椎动物和无脊椎动物免疫系统控制黄病毒和阿尔法病毒疾病的最新进展、当前挑战和未来前景。
{"title":"Generating prophylactic immunity against arboviruses in vertebrates and invertebrates","authors":"Daniel J. Rawle, Leon E. Hugo, Abigail L. Cox, Gregor J. Devine, Andreas Suhrbier","doi":"10.1038/s41577-024-01016-6","DOIUrl":"10.1038/s41577-024-01016-6","url":null,"abstract":"The World Health Organization recently declared a global initiative to control arboviral diseases. These are mainly caused by pathogenic flaviviruses (such as dengue, yellow fever and Zika viruses) and alphaviruses (such as chikungunya and Venezuelan equine encephalitis viruses). Vaccines represent key interventions for these viruses, with licensed human and/or veterinary vaccines being available for several members of both genera. However, a hurdle for the licensing of new vaccines is the epidemic nature of many arboviruses, which presents logistical challenges for phase III efficacy trials. Furthermore, our ability to predict or measure the post-vaccination immune responses that are sufficient for subclinical outcomes post-infection is limited. Given that arboviruses are also subject to control by the immune system of their insect vectors, several approaches are now emerging that aim to augment antiviral immunity in mosquitoes, including Wolbachia infection, transgenic mosquitoes, insect-specific viruses and paratransgenesis. In this Review, we discuss recent advances, current challenges and future prospects in exploiting both vertebrate and invertebrate immune systems for the control of flaviviral and alphaviral diseases. In this Review, the authors discuss recent advances, current challenges and future prospects in exploiting both vertebrate and invertebrate immune systems for the control of flaviviral and alphaviral diseases.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"621-636"},"PeriodicalIF":67.7,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140343457","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 : 2024-04-02DOI: 10.1038/s41577-024-01014-8
Elizabeth R. Mann, Ying Ka Lam, Holm H. Uhlig
The short-chain fatty acids (SCFAs) butyrate, propionate and acetate are microbial metabolites and their availability in the gut and other organs is determined by environmental factors, such as diet and use of antibiotics, that shape the diversity and metabolism of the microbiota. SCFAs regulate epithelial barrier function as well as mucosal and systemic immunity via evolutionary conserved processes that involve G protein-coupled receptor signalling or histone deacetylase activity. Indicatively, the anti-inflammatory role of butyrate is mediated through direct effects on the differentiation of intestinal epithelial cells, phagocytes, B cells and plasma cells, and regulatory and effector T cells. Intestinally derived SCFAs also directly and indirectly affect immunity at extra-intestinal sites, such as the liver, the lungs, the reproductive tract and the brain, and have been implicated in a range of disorders, including infections, intestinal inflammation, autoimmunity, food allergies, asthma and responses to cancer therapies. An ecological understanding of microbial communities and their interrelated metabolic states, as well as the engineering of butyrogenic bacteria may support SCFA-focused interventions for the prevention and treatment of immune-mediated diseases. Short-chain fatty acids (SCFAs) are microbial metabolites that regulate mucosal barrier integrity and immune cell functions. This Review summarizes latest insights into how SCFA levels might determine inflammatory and allergic disease outcomes by controlling the crosstalk between diet, the microbiome and immunity.
短链脂肪酸（SCFAs）丁酸盐、丙酸盐和乙酸盐是微生物的代谢产物，它们在肠道和其他器官中的供应量取决于环境因素，如饮食和抗生素的使用，这些因素影响着微生物群的多样性和新陈代谢。SCFAs 通过涉及 G 蛋白偶联受体信号或组蛋白去乙酰化酶活性的进化保守过程来调节上皮屏障功能以及粘膜和全身免疫。有迹象表明，丁酸盐的抗炎作用是通过直接影响肠上皮细胞、吞噬细胞、B 细胞和浆细胞以及调节性和效应 T 细胞的分化来实现的。肠道衍生的 SCFAs 还直接或间接影响肠道外部位的免疫，如肝脏、肺、生殖道和大脑，并与一系列疾病有关，包括感染、肠道炎症、自身免疫、食物过敏、哮喘和对癌症疗法的反应。从生态学角度了解微生物群落及其相互关联的新陈代谢状态，以及丁酸菌工程学，可能有助于采取以 SCFA 为重点的干预措施，预防和治疗免疫介导的疾病。
{"title":"Short-chain fatty acids: linking diet, the microbiome and immunity","authors":"Elizabeth R. Mann, Ying Ka Lam, Holm H. Uhlig","doi":"10.1038/s41577-024-01014-8","DOIUrl":"10.1038/s41577-024-01014-8","url":null,"abstract":"The short-chain fatty acids (SCFAs) butyrate, propionate and acetate are microbial metabolites and their availability in the gut and other organs is determined by environmental factors, such as diet and use of antibiotics, that shape the diversity and metabolism of the microbiota. SCFAs regulate epithelial barrier function as well as mucosal and systemic immunity via evolutionary conserved processes that involve G protein-coupled receptor signalling or histone deacetylase activity. Indicatively, the anti-inflammatory role of butyrate is mediated through direct effects on the differentiation of intestinal epithelial cells, phagocytes, B cells and plasma cells, and regulatory and effector T cells. Intestinally derived SCFAs also directly and indirectly affect immunity at extra-intestinal sites, such as the liver, the lungs, the reproductive tract and the brain, and have been implicated in a range of disorders, including infections, intestinal inflammation, autoimmunity, food allergies, asthma and responses to cancer therapies. An ecological understanding of microbial communities and their interrelated metabolic states, as well as the engineering of butyrogenic bacteria may support SCFA-focused interventions for the prevention and treatment of immune-mediated diseases. Short-chain fatty acids (SCFAs) are microbial metabolites that regulate mucosal barrier integrity and immune cell functions. This Review summarizes latest insights into how SCFA levels might determine inflammatory and allergic disease outcomes by controlling the crosstalk between diet, the microbiome and immunity.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"577-595"},"PeriodicalIF":67.7,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140343378","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 : 2024-03-28DOI: 10.1038/s41577-024-01028-2
Sizun Jiang
Sizun Jiang (while in the Garry Nolan lab) describes a method termed PANINI that allows simultaneous detection of nucleic acids at low copy numbers and protein markers in intact tissues, offering valuable insights into virus–immune system interactions and beyond.
{"title":"PANINI: Combined protein and nucleic acid imaging in tissues","authors":"Sizun Jiang","doi":"10.1038/s41577-024-01028-2","DOIUrl":"10.1038/s41577-024-01028-2","url":null,"abstract":"Sizun Jiang (while in the Garry Nolan lab) describes a method termed PANINI that allows simultaneous detection of nucleic acids at low copy numbers and protein markers in intact tissues, offering valuable insights into virus–immune system interactions and beyond.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"379-379"},"PeriodicalIF":67.7,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140310746","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 : 2024-03-19DOI: 10.1038/s41577-024-01024-6
Kirsty Minton
A study in Science reports 10 individuals with pre-TCRα deficiency who have late-onset or no clinical phenotype, which suggests that αβ T cells can develop through a pre-TCRα-independent, non-canonical rescue pathway.
科学》（Science）杂志上的一项研究报告了 10 名前 TCRα 缺乏症患者，他们发病较晚或没有临床表型，这表明αβ T 细胞可以通过前 TCRα 无关的非经典拯救途径发育。
{"title":"A pre-TCRα-independent pathway of αβ T cell differentiation","authors":"Kirsty Minton","doi":"10.1038/s41577-024-01024-6","DOIUrl":"10.1038/s41577-024-01024-6","url":null,"abstract":"A study in Science reports 10 individuals with pre-TCRα deficiency who have late-onset or no clinical phenotype, which suggests that αβ T cells can develop through a pre-TCRα-independent, non-canonical rescue pathway.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"305-305"},"PeriodicalIF":67.7,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140175699","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 : 2024-03-15DOI: 10.1038/s41577-024-01003-x
Madelon M. E. de Jong, Lanpeng Chen, Marc H. G. P. Raaijmakers, Tom Cupedo
Tissue inflammation is a hallmark of tumour microenvironments. In the bone marrow, tumour-associated inflammation impacts normal niches for haematopoietic progenitor cells and mature immune cells and supports the outgrowth and survival of malignant cells residing in these niche compartments. This Review provides an overview of our current understanding of inflammatory changes in the bone marrow microenvironment of myeloid and lymphoid malignancies, using acute myeloid leukaemia and multiple myeloma as examples and highlights unique and shared features of inflammation in niches for progenitor cells and plasma cells. Importantly, inflammation exerts profoundly different effects on normal bone marrow niches in these malignancies, and we provide context for possible drivers of these divergent effects. We explore the role of tumour cells in inflammatory changes, as well as the role of cellular constituents of normal bone marrow niches, including myeloid cells and stromal cells. Integrating knowledge of disease-specific dynamics of malignancy-associated bone marrow inflammation will provide a necessary framework for future targeting of these processes to improve patient outcome. Haematological malignancies are associated with inflammation in the bone marrow. In this Review, the authors discuss how tumour-associated inflammation affects the normal functions of the bone marrow and supports the outgrowth and survival of malignant cells. Moreover, they describe how the inflammatory changes in the bone marrow differ in myeloid and lymphoid malignancies.
{"title":"Bone marrow inflammation in haematological malignancies","authors":"Madelon M. E. de Jong, Lanpeng Chen, Marc H. G. P. Raaijmakers, Tom Cupedo","doi":"10.1038/s41577-024-01003-x","DOIUrl":"10.1038/s41577-024-01003-x","url":null,"abstract":"Tissue inflammation is a hallmark of tumour microenvironments. In the bone marrow, tumour-associated inflammation impacts normal niches for haematopoietic progenitor cells and mature immune cells and supports the outgrowth and survival of malignant cells residing in these niche compartments. This Review provides an overview of our current understanding of inflammatory changes in the bone marrow microenvironment of myeloid and lymphoid malignancies, using acute myeloid leukaemia and multiple myeloma as examples and highlights unique and shared features of inflammation in niches for progenitor cells and plasma cells. Importantly, inflammation exerts profoundly different effects on normal bone marrow niches in these malignancies, and we provide context for possible drivers of these divergent effects. We explore the role of tumour cells in inflammatory changes, as well as the role of cellular constituents of normal bone marrow niches, including myeloid cells and stromal cells. Integrating knowledge of disease-specific dynamics of malignancy-associated bone marrow inflammation will provide a necessary framework for future targeting of these processes to improve patient outcome. Haematological malignancies are associated with inflammation in the bone marrow. In this Review, the authors discuss how tumour-associated inflammation affects the normal functions of the bone marrow and supports the outgrowth and survival of malignant cells. Moreover, they describe how the inflammatory changes in the bone marrow differ in myeloid and lymphoid malignancies.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"543-558"},"PeriodicalIF":67.7,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140139357","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 : 2024-03-14DOI: 10.1038/s41577-024-01008-6
Markus F. Neurath
Cytokines produced by immune cells contribute to the development and perpetuation of inflammatory bowel disease (IBD), namely Crohn’s disease and ulcerative colitis, by regulating various aspects of the inflammatory response. Pro-inflammatory cytokines trigger chronic intestinal inflammation, tissue damage, carcinogenesis and perpetuation of disease and suppress the resolution of inflammation in IBD. The clinical success of antibodies that neutralize tumour necrosis factor (TNF) and the cytokine IL-12p40 in individuals with IBD has underscored this concept. Moreover, genetic and preclinical studies have emphasized the crucial role of IL-23 in IBD, leading to clinical approval of antibodies targeting this cytokine. Multiple studies have also investigated the administration of cytokines with assumed anti-inflammatory effects, but this approach has yet to show any real clinical benefit in individuals with IBD. Recent studies have targeted the cytokine network through the use of multi-cytokine blockers (for example, Janus kinase (JAK) inhibitors), IL-2-induced regulatory T cells or advanced combination therapies that use multiple cytokine blockers simultaneously (for example, anti-TNF along with anti-IL-23 antibodies). This Review will focus on our current understanding of how cytokines produced by innate and adaptive immune cells contribute to IBD pathogenesis and discuss how their modulation may inform future treatments for IBD. This Review explains how cytokines contribute to the pathogenesis of inflammatory bowel disease (IBD). The author highlights the cytokine-targeting drugs that are already being successfully used in the clinic and discusses the potential of other cytokine-modulating drugs in IBD.
{"title":"Strategies for targeting cytokines in inflammatory bowel disease","authors":"Markus F. Neurath","doi":"10.1038/s41577-024-01008-6","DOIUrl":"10.1038/s41577-024-01008-6","url":null,"abstract":"Cytokines produced by immune cells contribute to the development and perpetuation of inflammatory bowel disease (IBD), namely Crohn’s disease and ulcerative colitis, by regulating various aspects of the inflammatory response. Pro-inflammatory cytokines trigger chronic intestinal inflammation, tissue damage, carcinogenesis and perpetuation of disease and suppress the resolution of inflammation in IBD. The clinical success of antibodies that neutralize tumour necrosis factor (TNF) and the cytokine IL-12p40 in individuals with IBD has underscored this concept. Moreover, genetic and preclinical studies have emphasized the crucial role of IL-23 in IBD, leading to clinical approval of antibodies targeting this cytokine. Multiple studies have also investigated the administration of cytokines with assumed anti-inflammatory effects, but this approach has yet to show any real clinical benefit in individuals with IBD. Recent studies have targeted the cytokine network through the use of multi-cytokine blockers (for example, Janus kinase (JAK) inhibitors), IL-2-induced regulatory T cells or advanced combination therapies that use multiple cytokine blockers simultaneously (for example, anti-TNF along with anti-IL-23 antibodies). This Review will focus on our current understanding of how cytokines produced by innate and adaptive immune cells contribute to IBD pathogenesis and discuss how their modulation may inform future treatments for IBD. This Review explains how cytokines contribute to the pathogenesis of inflammatory bowel disease (IBD). The author highlights the cytokine-targeting drugs that are already being successfully used in the clinic and discusses the potential of other cytokine-modulating drugs in IBD.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"559-576"},"PeriodicalIF":67.7,"publicationDate":"2024-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140132091","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 : 2024-03-13DOI: 10.1038/s41577-024-01023-7
Laure F. Pittet, Christie C. A. Noble, Nicole L. Messina, Nigel Curtis
{"title":"Author Correction: Using BCG vaccination to protect against COVID-19: when reality fails to meet expectation","authors":"Laure F. Pittet, Christie C. A. Noble, Nicole L. Messina, Nigel Curtis","doi":"10.1038/s41577-024-01023-7","DOIUrl":"10.1038/s41577-024-01023-7","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"304-304"},"PeriodicalIF":67.7,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41577-024-01023-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140120170","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 : 2024-03-11DOI: 10.1038/s41577-024-00998-7
James W. Swann, Oakley C. Olson, Emmanuelle Passegué
Definitive haematopoiesis is the process by which haematopoietic stem cells, located in the bone marrow, generate all haematopoietic cell lineages in healthy adults. Although highly regulated to maintain a stable output of blood cells in health, the haematopoietic system is capable of extensive remodelling in response to external challenges, prioritizing the production of certain cell types at the expense of others. In this Review, we consider how acute insults, such as infections and cytotoxic drug-induced myeloablation, cause molecular, cellular and metabolic changes in haematopoietic stem and progenitor cells at multiple levels of the haematopoietic hierarchy to drive accelerated production of the mature myeloid cells needed to resolve the initiating insult. Moreover, we discuss how dysregulation or subversion of these emergency myelopoiesis mechanisms contributes to the progression of chronic inflammatory diseases and cancer. Acute infection and other insults cause extensive remodelling in the bone marrow to drive the production of new blood cells, often prioritizing the production of mature myeloid cells at the expense of other blood cell types. Here, the authors describe how haematopoiesis is affected by acute demand and how this can contribute to inflammatory disease and cancer when dysregulated.
{"title":"Made to order: emergency myelopoiesis and demand-adapted innate immune cell production","authors":"James W. Swann, Oakley C. Olson, Emmanuelle Passegué","doi":"10.1038/s41577-024-00998-7","DOIUrl":"10.1038/s41577-024-00998-7","url":null,"abstract":"Definitive haematopoiesis is the process by which haematopoietic stem cells, located in the bone marrow, generate all haematopoietic cell lineages in healthy adults. Although highly regulated to maintain a stable output of blood cells in health, the haematopoietic system is capable of extensive remodelling in response to external challenges, prioritizing the production of certain cell types at the expense of others. In this Review, we consider how acute insults, such as infections and cytotoxic drug-induced myeloablation, cause molecular, cellular and metabolic changes in haematopoietic stem and progenitor cells at multiple levels of the haematopoietic hierarchy to drive accelerated production of the mature myeloid cells needed to resolve the initiating insult. Moreover, we discuss how dysregulation or subversion of these emergency myelopoiesis mechanisms contributes to the progression of chronic inflammatory diseases and cancer. Acute infection and other insults cause extensive remodelling in the bone marrow to drive the production of new blood cells, often prioritizing the production of mature myeloid cells at the expense of other blood cell types. Here, the authors describe how haematopoiesis is affected by acute demand and how this can contribute to inflammatory disease and cancer when dysregulated.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"596-613"},"PeriodicalIF":67.7,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140096958","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 : 2024-03-11DOI: 10.1038/s41577-024-01020-w
Alexandra Flemming
{"title":"Regulation of innate-like activities of neonatal CD8+ T cells","authors":"Alexandra Flemming","doi":"10.1038/s41577-024-01020-w","DOIUrl":"10.1038/s41577-024-01020-w","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"232-232"},"PeriodicalIF":67.7,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140102113","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 : 2024-03-11DOI: 10.1038/s41577-024-01021-9
Alexandra Flemming
{"title":"CARD8 kills CD4+ T cells in response to HIV entry","authors":"Alexandra Flemming","doi":"10.1038/s41577-024-01021-9","DOIUrl":"10.1038/s41577-024-01021-9","url":null,"abstract":"","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"232-232"},"PeriodicalIF":67.7,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140102112","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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