Pub Date : 2024-05-07DOI: 10.1038/s41577-024-01025-5
Iain Comerford, Shaun R. McColl
Leukocyte migration is a fundamental component of innate and adaptive immune responses as it governs the recruitment and localization of these motile cells, which is crucial for immune cell priming, effector functions, memory responses and immune regulation. This complex cellular trafficking system is controlled to a large extent via highly regulated production of secreted chemokines and the restricted expression of their membrane-tethered G-protein-coupled receptors. The activity of chemokines and their receptors is also regulated by a subfamily of molecules known as atypical chemokine receptors (ACKRs), which are chemokine receptor-like molecules that do not couple to the classical signalling pathways that promote cell migration in response to chemokine ligation. There has been a great deal of progress in understanding the biology of these receptors and their functions in the immune system in the past decade. Here, we describe the contribution of the various ACKRs to innate and adaptive immune responses, focussing specifically on recent progress. This includes recent findings that have defined the role for ACKRs in sculpting extracellular chemokine gradients, findings that broaden the spectrum of chemokine ligands recognized by these receptors, candidate new additions to ACKR family, and our increasing understanding of the role of these receptors in shaping the migration of innate and adaptive immune cells. This Review from Comerford and McColl discusses recent advances that have been made in understanding the biology of the atypical chemokine receptor (ACKR) family. The authors explain how these receptors interact with their ligands to shape immune responses and also highlight potential new additions to the ACKR family.
白细胞迁移是先天性和适应性免疫反应的基本组成部分，因为它控制着这些运动细胞的招募和定位，这对免疫细胞的启动、效应功能、记忆反应和免疫调节至关重要。这种复杂的细胞运输系统在很大程度上是通过高度调节分泌型趋化因子的产生及其膜系 G 蛋白偶联受体的限制性表达来控制的。趋化因子及其受体的活性还受一个被称为非典型趋化因子受体（ACKRs）的分子亚家族的调控，ACKRs 是类似于趋化因子受体的分子，不与经典的信号通路耦合，这些信号通路在趋化因子的作用下促进细胞迁移。在过去十年中，人们在了解这些受体的生物学特性及其在免疫系统中的功能方面取得了很大进展。在这里，我们描述了各种 ACKR 对先天性和适应性免疫反应的贡献，并特别关注最近的进展。这包括最近确定 ACKR 在形成细胞外趋化因子梯度中的作用的研究结果、扩大这些受体识别的趋化因子配体范围的研究结果、ACKR 家族的候选新成员，以及我们对这些受体在形成先天性和适应性免疫细胞迁移中的作用的进一步了解。
{"title":"Atypical chemokine receptors in the immune system","authors":"Iain Comerford, Shaun R. McColl","doi":"10.1038/s41577-024-01025-5","DOIUrl":"10.1038/s41577-024-01025-5","url":null,"abstract":"Leukocyte migration is a fundamental component of innate and adaptive immune responses as it governs the recruitment and localization of these motile cells, which is crucial for immune cell priming, effector functions, memory responses and immune regulation. This complex cellular trafficking system is controlled to a large extent via highly regulated production of secreted chemokines and the restricted expression of their membrane-tethered G-protein-coupled receptors. The activity of chemokines and their receptors is also regulated by a subfamily of molecules known as atypical chemokine receptors (ACKRs), which are chemokine receptor-like molecules that do not couple to the classical signalling pathways that promote cell migration in response to chemokine ligation. There has been a great deal of progress in understanding the biology of these receptors and their functions in the immune system in the past decade. Here, we describe the contribution of the various ACKRs to innate and adaptive immune responses, focussing specifically on recent progress. This includes recent findings that have defined the role for ACKRs in sculpting extracellular chemokine gradients, findings that broaden the spectrum of chemokine ligands recognized by these receptors, candidate new additions to ACKR family, and our increasing understanding of the role of these receptors in shaping the migration of innate and adaptive immune cells. This Review from Comerford and McColl discusses recent advances that have been made in understanding the biology of the atypical chemokine receptor (ACKR) family. The authors explain how these receptors interact with their ligands to shape immune responses and also highlight potential new additions to the ACKR family.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"753-769"},"PeriodicalIF":67.7,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140845450","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 : 2024-05-02DOI: 10.1038/s41577-024-01029-1
Thi H. O. Nguyen, Louise C. Rowntree, Brendon Y. Chua, Ryan S. Thwaites, Katherine Kedzierska
Influenza A viruses remain a global threat to human health, with continued pandemic potential. In this Review, we discuss our current understanding of the optimal immune responses that drive recovery from influenza virus infection, highlighting the fine balance between protective immune mechanisms and detrimental immunopathology. We describe the contribution of innate and adaptive immune cells, inflammatory modulators and antibodies to influenza virus-specific immunity, inflammation and immunopathology. We highlight recent human influenza virus challenge studies that advance our understanding of susceptibility to influenza and determinants of symptomatic disease. We also describe studies of influenza virus-specific immunity in high-risk groups following infection and vaccination that inform the design of future vaccines to promote optimal antiviral immunity, particularly in vulnerable populations. Finally, we draw on lessons from the COVID-19 pandemic to refocus our attention to the ever-changing, highly mutable influenza A virus, predicted to cause future global pandemics. An optimal immune response to influenza virus strikes a balance between protective antiviral immune mechanisms and detrimental immunopathology. Here, the authors review the immune mechanisms responsible for each side of this balance and how this may inform future vaccine design.
{"title":"Defining the balance between optimal immunity and immunopathology in influenza virus infection","authors":"Thi H. O. Nguyen, Louise C. Rowntree, Brendon Y. Chua, Ryan S. Thwaites, Katherine Kedzierska","doi":"10.1038/s41577-024-01029-1","DOIUrl":"10.1038/s41577-024-01029-1","url":null,"abstract":"Influenza A viruses remain a global threat to human health, with continued pandemic potential. In this Review, we discuss our current understanding of the optimal immune responses that drive recovery from influenza virus infection, highlighting the fine balance between protective immune mechanisms and detrimental immunopathology. We describe the contribution of innate and adaptive immune cells, inflammatory modulators and antibodies to influenza virus-specific immunity, inflammation and immunopathology. We highlight recent human influenza virus challenge studies that advance our understanding of susceptibility to influenza and determinants of symptomatic disease. We also describe studies of influenza virus-specific immunity in high-risk groups following infection and vaccination that inform the design of future vaccines to promote optimal antiviral immunity, particularly in vulnerable populations. Finally, we draw on lessons from the COVID-19 pandemic to refocus our attention to the ever-changing, highly mutable influenza A virus, predicted to cause future global pandemics. An optimal immune response to influenza virus strikes a balance between protective antiviral immune mechanisms and detrimental immunopathology. Here, the authors review the immune mechanisms responsible for each side of this balance and how this may inform future vaccine design.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"720-735"},"PeriodicalIF":67.7,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140821097","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 : 2024-05-02DOI: 10.1038/s41577-024-01030-8
Tim R. Mosmann, Andrew J. McMichael, Alexandre LeVert, John W. McCauley, Jeffrey W. Almond
Vaccination remains our main defence against influenza, which causes substantial annual mortality and poses a serious pandemic threat. Influenza virus evades immunity by rapidly changing its surface antigens but, even when the vaccine is well matched to the current circulating virus strains, influenza vaccines are not as effective as many other vaccines. Influenza vaccine development has traditionally focused on the induction of protective antibodies, but there is mounting evidence that T cell responses are also protective against influenza. Thus, future vaccines designed to promote both broad T cell effector functions and antibodies may provide enhanced protection. As we discuss, such vaccines present several challenges that require new strategic and economic considerations. Vaccine-induced T cells relevant to protection may reside in the lungs or lymphoid tissues, requiring more invasive assays to assess the immunogenicity of vaccine candidates. T cell functions may contain and resolve infection rather than completely prevent infection and early illness, requiring vaccine effectiveness to be assessed based on the prevention of severe disease and death rather than symptomatic infection. It can be complex and costly to measure T cell responses and infrequent clinical outcomes, and thus innovations in clinical trial design are needed for economic reasons. Nevertheless, the goal of more effective influenza vaccines justifies renewed and intensive efforts. Compared with many other vaccines, current vaccines against influenza provide only limited protection. Here, the authors describe the challenges and recent attempts at generating T cell-based vaccines. It may be important to combine T cell-based vaccines with antibody-based vaccines to provide long-lasting immunity across influenza virus strains.
疫苗接种仍然是我们抵御流感的主要手段，流感每年造成大量死亡，并构成严重的大流行威胁。流感病毒通过迅速改变其表面抗原来逃避免疫，但即使疫苗与当前流行的病毒株非常匹配，流感疫苗也不如许多其他疫苗有效。流感疫苗的研发历来侧重于诱导保护性抗体，但越来越多的证据表明，T 细胞反应也对流感有保护作用。因此，未来旨在促进广泛的 T 细胞效应功能和抗体的疫苗可能会提供更强的保护。正如我们所讨论的，这类疫苗面临着一些挑战，需要新的战略和经济考量。疫苗诱导的与保护相关的 T 细胞可能存在于肺部或淋巴组织中，因此需要更多侵入性试验来评估候选疫苗的免疫原性。T 细胞功能可能会抑制和化解感染，而不是完全预防感染和早期疾病，这就要求根据预防严重疾病和死亡而不是无症状感染来评估疫苗的有效性。对 T 细胞反应和不常见的临床结果进行测量既复杂又昂贵，因此出于经济原因，需要对临床试验设计进行创新。尽管如此，为了实现更有效的流感疫苗这一目标，我们有理由继续加紧努力。
{"title":"Opportunities and challenges for T cell-based influenza vaccines","authors":"Tim R. Mosmann, Andrew J. McMichael, Alexandre LeVert, John W. McCauley, Jeffrey W. Almond","doi":"10.1038/s41577-024-01030-8","DOIUrl":"10.1038/s41577-024-01030-8","url":null,"abstract":"Vaccination remains our main defence against influenza, which causes substantial annual mortality and poses a serious pandemic threat. Influenza virus evades immunity by rapidly changing its surface antigens but, even when the vaccine is well matched to the current circulating virus strains, influenza vaccines are not as effective as many other vaccines. Influenza vaccine development has traditionally focused on the induction of protective antibodies, but there is mounting evidence that T cell responses are also protective against influenza. Thus, future vaccines designed to promote both broad T cell effector functions and antibodies may provide enhanced protection. As we discuss, such vaccines present several challenges that require new strategic and economic considerations. Vaccine-induced T cells relevant to protection may reside in the lungs or lymphoid tissues, requiring more invasive assays to assess the immunogenicity of vaccine candidates. T cell functions may contain and resolve infection rather than completely prevent infection and early illness, requiring vaccine effectiveness to be assessed based on the prevention of severe disease and death rather than symptomatic infection. It can be complex and costly to measure T cell responses and infrequent clinical outcomes, and thus innovations in clinical trial design are needed for economic reasons. Nevertheless, the goal of more effective influenza vaccines justifies renewed and intensive efforts. Compared with many other vaccines, current vaccines against influenza provide only limited protection. Here, the authors describe the challenges and recent attempts at generating T cell-based vaccines. It may be important to combine T cell-based vaccines with antibody-based vaccines to provide long-lasting immunity across influenza virus strains.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"736-752"},"PeriodicalIF":67.7,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140819429","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 : 2024-04-29DOI: 10.1038/s41577-024-01027-3
Yi Huang, Wei Jiang, Rongbin Zhou
Damage-associated molecular patterns (DAMPs) are endogenous molecules that are released from host cells as a result of cell death or damage. The release of DAMPs in tissues is associated with loss of tissue homeostasis. Sensing of DAMPs by innate immune receptors triggers inflammation, which can be beneficial in initiating the processes that restore tissue homeostasis but can also drive inflammatory diseases. In recent years, the sensing of intracellular DAMPs has received extensive attention in the field of sterile inflammation. However, emerging studies have shown that DAMPs that originate from neighbouring cells, and even from distal tissues or organs, also mediate sterile inflammatory responses. This multi-level sensing of DAMPs is crucial for intercellular, trans-tissue and trans-organ communication. Here, we summarize how DAMP-sensing receptors detect DAMPs from intracellular, intercellular or distal tissue and organ sources to mediate sterile inflammation. We also discuss the possibility of targeting DAMPs or their corresponding receptors to treat inflammatory diseases. Here, Rongbin Zhou and colleagues review the different types of damage-associated molecular pattern (DAMP) that trigger sterile inflammation via pattern recognition receptors. The authors group these DAMPs on the basis of whether they arise from inside cells, from neighbouring cells or from distant tissues, and they discuss the relevance of such DAMPs in various inflammatory disease settings.
{"title":"DAMP sensing and sterile inflammation: intracellular, intercellular and inter-organ pathways","authors":"Yi Huang, Wei Jiang, Rongbin Zhou","doi":"10.1038/s41577-024-01027-3","DOIUrl":"10.1038/s41577-024-01027-3","url":null,"abstract":"Damage-associated molecular patterns (DAMPs) are endogenous molecules that are released from host cells as a result of cell death or damage. The release of DAMPs in tissues is associated with loss of tissue homeostasis. Sensing of DAMPs by innate immune receptors triggers inflammation, which can be beneficial in initiating the processes that restore tissue homeostasis but can also drive inflammatory diseases. In recent years, the sensing of intracellular DAMPs has received extensive attention in the field of sterile inflammation. However, emerging studies have shown that DAMPs that originate from neighbouring cells, and even from distal tissues or organs, also mediate sterile inflammatory responses. This multi-level sensing of DAMPs is crucial for intercellular, trans-tissue and trans-organ communication. Here, we summarize how DAMP-sensing receptors detect DAMPs from intracellular, intercellular or distal tissue and organ sources to mediate sterile inflammation. We also discuss the possibility of targeting DAMPs or their corresponding receptors to treat inflammatory diseases. Here, Rongbin Zhou and colleagues review the different types of damage-associated molecular pattern (DAMP) that trigger sterile inflammation via pattern recognition receptors. The authors group these DAMPs on the basis of whether they arise from inside cells, from neighbouring cells or from distant tissues, and they discuss the relevance of such DAMPs in various inflammatory disease settings.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"703-719"},"PeriodicalIF":67.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140814463","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 : 2024-04-26DOI: 10.1038/s41577-024-01038-0
Robyn Loves, Eyal Grunebaum
A preprint by Yi et al. shows a role for the FAS signalling pathway in controlling the persistence of CAR-modified lymphocytes.
Yi等人的预印本显示了FAS信号通路在控制CAR修饰淋巴细胞的持久性方面的作用。
{"title":"FAS signalling pathway is crucial for CAR T cell persistence","authors":"Robyn Loves, Eyal Grunebaum","doi":"10.1038/s41577-024-01038-0","DOIUrl":"10.1038/s41577-024-01038-0","url":null,"abstract":"A preprint by Yi et al. shows a role for the FAS signalling pathway in controlling the persistence of CAR-modified lymphocytes.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"380-380"},"PeriodicalIF":67.7,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140648700","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 : 2024-04-26DOI: 10.1038/s41577-024-01039-z
Kirsty Minton
Wei et al. report a role for membrane perforation mediated by gasdermin D pores in disruption of the blood–brain barrier.
Wei 等人报告了由气孔 D 介导的膜穿孔在破坏血脑屏障中的作用。
{"title":"Noncanonical inflammasome mediates BBB breakdown","authors":"Kirsty Minton","doi":"10.1038/s41577-024-01039-z","DOIUrl":"10.1038/s41577-024-01039-z","url":null,"abstract":"Wei et al. report a role for membrane perforation mediated by gasdermin D pores in disruption of the blood–brain barrier.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"378-378"},"PeriodicalIF":67.7,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140648777","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 : 2024-04-24DOI: 10.1038/s41577-024-01022-8
Karen E. Martin, Quirin Hammer, Karlo Perica, Michel Sadelain, Karl-Johan Malmberg
Allogeneic cellular immunotherapies hold a great promise for cancer treatment owing to their potential cost-effectiveness, scalability and on-demand availability. However, immune rejection of adoptively transferred allogeneic T and natural killer (NK) cells is a substantial obstacle to achieving clinical responses that are comparable to responses obtained with current autologous chimeric antigen receptor T cell therapies. In this Perspective, we discuss strategies to confer cell-intrinsic, immune-evasive properties to allogeneic T cells and NK cells in order to prevent or delay their immune rejection, thereby widening the therapeutic window. We discuss how common viral and cancer immune escape mechanisms can serve as a blueprint for improving the persistence of off-the-shelf allogeneic cell therapies. The prospects of harnessing genome editing and synthetic biology to design cell-based precision immunotherapies extend beyond programming target specificities and require careful consideration of innate and adaptive responses in the recipient that may curtail the biodistribution, in vivo expansion and persistence of cellular therapeutics. Genome editing approaches can be used to confer immune-evasive properties to allogeneic cellular immunotherapies, with the aim of achieving persistent responses and efficiencies that are comparable to those of autologous chimeric antigen receptor T cell therapies. This Perspective discusses how current knowledge about viral or tumour immune evasion could be incorporated into the design of off-the-shelf tumour-specific T and NK cells for the production of cost-effective and scalable cancer immunotherapies.
{"title":"Engineering immune-evasive allogeneic cellular immunotherapies","authors":"Karen E. Martin, Quirin Hammer, Karlo Perica, Michel Sadelain, Karl-Johan Malmberg","doi":"10.1038/s41577-024-01022-8","DOIUrl":"10.1038/s41577-024-01022-8","url":null,"abstract":"Allogeneic cellular immunotherapies hold a great promise for cancer treatment owing to their potential cost-effectiveness, scalability and on-demand availability. However, immune rejection of adoptively transferred allogeneic T and natural killer (NK) cells is a substantial obstacle to achieving clinical responses that are comparable to responses obtained with current autologous chimeric antigen receptor T cell therapies. In this Perspective, we discuss strategies to confer cell-intrinsic, immune-evasive properties to allogeneic T cells and NK cells in order to prevent or delay their immune rejection, thereby widening the therapeutic window. We discuss how common viral and cancer immune escape mechanisms can serve as a blueprint for improving the persistence of off-the-shelf allogeneic cell therapies. The prospects of harnessing genome editing and synthetic biology to design cell-based precision immunotherapies extend beyond programming target specificities and require careful consideration of innate and adaptive responses in the recipient that may curtail the biodistribution, in vivo expansion and persistence of cellular therapeutics. Genome editing approaches can be used to confer immune-evasive properties to allogeneic cellular immunotherapies, with the aim of achieving persistent responses and efficiencies that are comparable to those of autologous chimeric antigen receptor T cell therapies. This Perspective discusses how current knowledge about viral or tumour immune evasion could be incorporated into the design of off-the-shelf tumour-specific T and NK cells for the production of cost-effective and scalable cancer immunotherapies.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"680-693"},"PeriodicalIF":67.7,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639949","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 : 2024-04-24DOI: 10.1038/s41577-024-01036-2
Lucy Bird
Sex hormones in male mice negatively regulate type 2 innate lymphoid cells in the skin, impairing the induction and activation of dendritic cells and thereby contributing to differences in immunity in males and females.
{"title":"Weaker skin immunity in males due to androgen effects on ILC2s","authors":"Lucy Bird","doi":"10.1038/s41577-024-01036-2","DOIUrl":"10.1038/s41577-024-01036-2","url":null,"abstract":"Sex hormones in male mice negatively regulate type 2 innate lymphoid cells in the skin, impairing the induction and activation of dendritic cells and thereby contributing to differences in immunity in males and females.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"377-377"},"PeriodicalIF":67.7,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639738","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 : 2024-04-24DOI: 10.1038/s41577-024-01037-1
Adrian Liston
Adrian Liston, professor of pathology at the University of Cambridge, UK, has published several illustrated children’s books on the topic of vaccination and has developed a computer game called ‘VirusFighter’. Here, he shares his thoughts on how to become an effective science communicator.
{"title":"Harnessing our lived experience for science communication","authors":"Adrian Liston","doi":"10.1038/s41577-024-01037-1","DOIUrl":"10.1038/s41577-024-01037-1","url":null,"abstract":"Adrian Liston, professor of pathology at the University of Cambridge, UK, has published several illustrated children’s books on the topic of vaccination and has developed a computer game called ‘VirusFighter’. Here, he shares his thoughts on how to become an effective science communicator.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"375-376"},"PeriodicalIF":67.7,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140639886","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 : 2024-04-22DOI: 10.1038/s41577-024-01026-4
Mara De Martino, Jeffrey C. Rathmell, Lorenzo Galluzzi, Claire Vanpouille-Box
Accumulating evidence suggests that metabolic rewiring in malignant cells supports tumour progression not only by providing cancer cells with increased proliferative potential and an improved ability to adapt to adverse microenvironmental conditions but also by favouring the evasion of natural and therapy-driven antitumour immune responses. Here, we review cancer cell-intrinsic and cancer cell-extrinsic mechanisms through which alterations of metabolism in malignant cells interfere with innate and adaptive immune functions in support of accelerated disease progression. Further, we discuss the potential of targeting such alterations to enhance anticancer immunity for therapeutic purposes. This Review discusses the mechanisms by which common alterations of cancer cell metabolism interfere with immune functions to promote immunoevasion and tumour progression, and avenues to target such alterations for therapeutic purposes.
{"title":"Cancer cell metabolism and antitumour immunity","authors":"Mara De Martino, Jeffrey C. Rathmell, Lorenzo Galluzzi, Claire Vanpouille-Box","doi":"10.1038/s41577-024-01026-4","DOIUrl":"10.1038/s41577-024-01026-4","url":null,"abstract":"Accumulating evidence suggests that metabolic rewiring in malignant cells supports tumour progression not only by providing cancer cells with increased proliferative potential and an improved ability to adapt to adverse microenvironmental conditions but also by favouring the evasion of natural and therapy-driven antitumour immune responses. Here, we review cancer cell-intrinsic and cancer cell-extrinsic mechanisms through which alterations of metabolism in malignant cells interfere with innate and adaptive immune functions in support of accelerated disease progression. Further, we discuss the potential of targeting such alterations to enhance anticancer immunity for therapeutic purposes. This Review discusses the mechanisms by which common alterations of cancer cell metabolism interfere with immune functions to promote immunoevasion and tumour progression, and avenues to target such alterations for therapeutic purposes.","PeriodicalId":19049,"journal":{"name":"Nature Reviews Immunology","volume":" ","pages":"654-669"},"PeriodicalIF":67.7,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140637553","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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