Pub Date : 2024-10-31DOI: 10.1016/j.coi.2024.102499
Daniel Min , Jacob Fiedler , Niroshana Anandasabapathy
As cancer immunotherapy evolves, tissue-resident memory (TRM) cells remain key contributors to the antitumoral immune response due to their ability to mediate local tumor control, high expression of immune checkpoints, potential to respond to immunotherapy, and location across tissue sites where distal tumor metastases occur. This review synthesizes recent findings on the biology of TRM cells, their role in cancer, and their interactions with the tumor microenvironment. We also identify several critical research gaps, such as how mechanistic interrogation of TRM cell function is required for integration into therapeutics, proposing a focused research agenda to better exploit their potential.
{"title":"Tissue-resident memory cells in antitumoral immunity and cancer immunotherapy","authors":"Daniel Min , Jacob Fiedler , Niroshana Anandasabapathy","doi":"10.1016/j.coi.2024.102499","DOIUrl":"10.1016/j.coi.2024.102499","url":null,"abstract":"<div><div>As cancer immunotherapy evolves, tissue-resident memory (T<sub>RM</sub>) cells remain key contributors to the antitumoral immune response due to their ability to mediate local tumor control, high expression of immune checkpoints, potential to respond to immunotherapy, and location across tissue sites where distal tumor metastases occur. This review synthesizes recent findings on the biology of T<sub>RM</sub> cells, their role in cancer, and their interactions with the tumor microenvironment. We also identify several critical research gaps, such as how mechanistic interrogation of T<sub>RM</sub> cell function is required for integration into therapeutics, proposing a focused research agenda to better exploit their potential.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142561113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-29DOI: 10.1016/j.coi.2024.102500
Christopher A Tibbitt , Jonathan M Coquet
Allergic diseases continue to increase in prevalence across the globe. Decades of research has uncovered the cytokines and transcription factors that are central to the allergic immune response, but only in the last few years have we begun to understand the metabolic requirements of allergic immunity. Here, we discuss the metabolic features of so-called ‘type 2’ lymphocytes, which are heavily implicated in allergy. We highlight the central role that nuclear receptors, such as peroxisome proliferator–activated receptor gamma, play in type 2 lymphocyte biology and explore the influence of dietary and microbial factors in allergic inflammation. In the future, targeting metabolic checkpoints may offer a meaningful way of treating patients with allergic disorders.
{"title":"Metabolic requirements of type 2 lymphocytes in allergic disease","authors":"Christopher A Tibbitt , Jonathan M Coquet","doi":"10.1016/j.coi.2024.102500","DOIUrl":"10.1016/j.coi.2024.102500","url":null,"abstract":"<div><div>Allergic diseases continue to increase in prevalence across the globe. Decades of research has uncovered the cytokines and transcription factors that are central to the allergic immune response, but only in the last few years have we begun to understand the metabolic requirements of allergic immunity. Here, we discuss the metabolic features of so-called ‘type 2’ lymphocytes, which are heavily implicated in allergy. We highlight the central role that nuclear receptors, such as peroxisome proliferator–activated receptor gamma, play in type 2 lymphocyte biology and explore the influence of dietary and microbial factors in allergic inflammation. In the future, targeting metabolic checkpoints may offer a meaningful way of treating patients with allergic disorders.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142538692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-26DOI: 10.1016/j.coi.2024.102498
Pierpaolo Ginefra , Helen C Hope , Girieca Lorusso , Patrizia D’Amelio , Nicola Vannini
Aging is one of the greatest risk factors for several chronic diseases and is accompanied by a progressive decline of cellular and organ function. Recent studies have highlighted the changes in metabolism as one of the main drivers of organism dysfunctions during aging and how that strongly deteriorate immune cell performance and function. Indeed, a dysfunctional immune system has been shown to have a pleiotropic impact on the organism, accelerating the overall aging process of an individual.
Intrinsic and extrinsic factors are responsible for such metabolic alterations. Understanding the contribution, regulation, and connection of these different factors is fundamental to comprehend the process of aging and develop approaches to mitigate age-related immune decline. Here, we describe metabolic perturbations occurring at cellular and systemic levels. Particularly, we emphasize the interplay between metabolism and immunosenescence and describe novel interventions to protect immune function and promote health span.
{"title":"The immunometabolic roots of aging","authors":"Pierpaolo Ginefra , Helen C Hope , Girieca Lorusso , Patrizia D’Amelio , Nicola Vannini","doi":"10.1016/j.coi.2024.102498","DOIUrl":"10.1016/j.coi.2024.102498","url":null,"abstract":"<div><div>Aging is one of the greatest risk factors for several chronic diseases and is accompanied by a progressive decline of cellular and organ function. Recent studies have highlighted the changes in metabolism as one of the main drivers of organism dysfunctions during aging and how that strongly deteriorate immune cell performance and function. Indeed, a dysfunctional immune system has been shown to have a pleiotropic impact on the organism, accelerating the overall aging process of an individual.</div><div>Intrinsic and extrinsic factors are responsible for such metabolic alterations. Understanding the contribution, regulation, and connection of these different factors is fundamental to comprehend the process of aging and develop approaches to mitigate age-related immune decline. Here, we describe metabolic perturbations occurring at cellular and systemic levels. Particularly, we emphasize the interplay between metabolism and immunosenescence and describe novel interventions to protect immune function and promote health span.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-09DOI: 10.1016/j.coi.2024.102472
Janelle S Ayres
Successful treatment of infectious diseases requires a multiprong approach involving strategies that limit pathogen burdens and that limit disease. Traditionally, disease defense is thought to be a direct function of pathogen killing, and thus, our current methods for treating infections have largely relied on pathogen eradication, leading to drug resistance. Strategies that target the virulence of the pathogen, called antivirulence, have been proposed to be a necessary strategy to integrate into our infectious disease toolbox to promote disease defense and alleviate the burden of drug resistance. Traditional antivirulence strategies have largely focused on developing compounds that directly target microbial virulence factors or products to impair their ability to initiate and sustain infection. As virulence is linked to pathogen fitness, simply targeting a virulence factor may not be sufficient to overcome the ability of pathogens evolving resistance. In this review, I discuss co-operative defenses that hosts have evolved to promote antivirulence mechanisms that suppress pathogen virulence without having a negative impact on pathogen fitness. I also discuss the different definitions antivirulence has been assigned over the years and suggest a more holistic one. Co-operative defenses remain an underexplored resource in medicine, and by learning from how hosts have evolved to promote antivirulence, we have the potential to develop disease defense interventions without the risk of pathogens developing drug resistance.
{"title":"Host-encoded antivirulence defenses: host physiologies teach pathogens to play nice","authors":"Janelle S Ayres","doi":"10.1016/j.coi.2024.102472","DOIUrl":"10.1016/j.coi.2024.102472","url":null,"abstract":"<div><div>Successful treatment of infectious diseases requires a multiprong approach involving strategies that limit pathogen burdens and that limit disease. Traditionally, disease defense is thought to be a direct function of pathogen killing, and thus, our current methods for treating infections have largely relied on pathogen eradication, leading to drug resistance. Strategies that target the virulence of the pathogen, called antivirulence, have been proposed to be a necessary strategy to integrate into our infectious disease toolbox to promote disease defense and alleviate the burden of drug resistance. Traditional antivirulence strategies have largely focused on developing compounds that directly target microbial virulence factors or products to impair their ability to initiate and sustain infection. As virulence is linked to pathogen fitness, simply targeting a virulence factor may not be sufficient to overcome the ability of pathogens evolving resistance. In this review, I discuss co-operative defenses that hosts have evolved to promote antivirulence mechanisms that suppress pathogen virulence without having a negative impact on pathogen fitness. I also discuss the different definitions antivirulence has been assigned over the years and suggest a more holistic one. Co-operative defenses remain an underexplored resource in medicine, and by learning from how hosts have evolved to promote antivirulence, we have the potential to develop disease defense interventions without the risk of pathogens developing drug resistance.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-04DOI: 10.1016/j.coi.2024.102491
Hannah Yang , Chan Kim , Weiping Zou
Tumor-associated macrophages (TAMs) constitute the primary subset of immune cells within the tumor microenvironment (TME). Exhibiting both phenotypic and functional heterogeneity, TAMs play distinct roles in tumor initiation, progression, and responses to therapy in patients with cancer. In response to various immune and metabolic cues within the TME, TAMs dynamically alter their metabolic profiles to adapt. Changes in glucose, amino acid, and lipid metabolism in TAMs, as well as their interaction with oncometabolites, not only sustain their energy demands but also influence their impact on tumor immune responses. Understanding the molecular mechanisms underlying the metabolic reprogramming of TAMs and their orchestration of metabolic processes can offer insights for the development of novel cancer immunotherapies targeting TAMs. Here, we discuss how metabolism reprograms macrophages in the TME and review clinical trials aiming to normalize metabolic alterations in TAMs and alleviate TAM-mediated immune suppression and protumor activity.
{"title":"Metabolism and macrophages in the tumor microenvironment","authors":"Hannah Yang , Chan Kim , Weiping Zou","doi":"10.1016/j.coi.2024.102491","DOIUrl":"10.1016/j.coi.2024.102491","url":null,"abstract":"<div><div>Tumor-associated macrophages (TAMs) constitute the primary subset of immune cells within the tumor microenvironment (TME). Exhibiting both phenotypic and functional heterogeneity, TAMs play distinct roles in tumor initiation, progression, and responses to therapy in patients with cancer. In response to various immune and metabolic cues within the TME, TAMs dynamically alter their metabolic profiles to adapt. Changes in glucose, amino acid, and lipid metabolism in TAMs, as well as their interaction with oncometabolites, not only sustain their energy demands but also influence their impact on tumor immune responses. Understanding the molecular mechanisms underlying the metabolic reprogramming of TAMs and their orchestration of metabolic processes can offer insights for the development of novel cancer immunotherapies targeting TAMs. Here, we discuss how metabolism reprograms macrophages in the TME and review clinical trials aiming to normalize metabolic alterations in TAMs and alleviate TAM-mediated immune suppression and protumor activity.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-03DOI: 10.1016/j.coi.2024.102497
Jorgo Lika , Jing Fan
Neutrophils, the first responders of the innate immune system, can turn on a range of effector functions upon activation. Emerging research shows activated neutrophils undergo highly dynamic metabolic rewiring. This metabolic rewiring provides energy and reducing power to fuel effector functions and modulate signaling molecules to regulate neutrophil functions. Here, we review the current understanding of the specific metabolic requirements and regulators of neutrophil migration, neutrophil extracellular traps release, and pathogen killing. Particularly, we discuss how major carbohydrate metabolic pathways, including glycolysis, glycogen cycling, pentose phosphate pathway, and TCA cycle, are rewired upon neutrophil activation to support these functions. Continued investigation into the metabolic regulators of neutrophil functions can lead to therapeutic opportunities in various diseases.
{"title":"Carbohydrate metabolism in supporting and regulating neutrophil effector functions","authors":"Jorgo Lika , Jing Fan","doi":"10.1016/j.coi.2024.102497","DOIUrl":"10.1016/j.coi.2024.102497","url":null,"abstract":"<div><div>Neutrophils, the first responders of the innate immune system, can turn on a range of effector functions upon activation. Emerging research shows activated neutrophils undergo highly dynamic metabolic rewiring. This metabolic rewiring provides energy and reducing power to fuel effector functions and modulate signaling molecules to regulate neutrophil functions. Here, we review the current understanding of the specific metabolic requirements and regulators of neutrophil migration, neutrophil extracellular traps release, and pathogen killing. Particularly, we discuss how major carbohydrate metabolic pathways, including glycolysis, glycogen cycling, pentose phosphate pathway, and TCA cycle, are rewired upon neutrophil activation to support these functions. Continued investigation into the metabolic regulators of neutrophil functions can lead to therapeutic opportunities in various diseases.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142376471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 10.1016/j.coi.2024.102485
Daehong Kim , Jaemin Kim , Hyeonuk Yeo , Yeonseok Chung
Aging, metabolism, and immunity have long been considered distinct domains. Aging is primarily associated with the gradual decline of physiological functions, metabolism regulates energy production and maintains cellular processes, and the immune system manages innate and adaptive responses against pathogens and vaccines. However, recent studies have revealed that these three systems are intricately interconnected, collectively influencing an individual’s response to stress and disease. This review explores the interplay between immunometabolism, T follicular helper cells, B cells, and aging, focusing on how these interactions impact immune function in the elderly.
{"title":"Immunometabolic regulation of germinal centers and its implications for aging","authors":"Daehong Kim , Jaemin Kim , Hyeonuk Yeo , Yeonseok Chung","doi":"10.1016/j.coi.2024.102485","DOIUrl":"10.1016/j.coi.2024.102485","url":null,"abstract":"<div><div>Aging, metabolism, and immunity have long been considered distinct domains. Aging is primarily associated with the gradual decline of physiological functions, metabolism regulates energy production and maintains cellular processes, and the immune system manages innate and adaptive responses against pathogens and vaccines. However, recent studies have revealed that these three systems are intricately interconnected, collectively influencing an individual’s response to stress and disease. This review explores the interplay between immunometabolism, T follicular helper cells, B cells, and aging, focusing on how these interactions impact immune function in the elderly.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 10.1016/j.coi.2024.102495
William J Branchett , Margarida Saraiva , Anne O’Garra
Intricate immune regulation is required at mucosal surfaces to allow tolerance to microbiota and harmless allergens and to prevent overexuberant inflammatory responses to pathogens. The cytokine Interleukin-10 (IL-10) is a key mediator of mucosal immune regulation. While IL-10 can be produced by virtually all cells of the immune system, many of its in vivo functions depend upon its production by regulatory or effector T cell populations and its signalling to macrophages, dendritic cells and specific T cell subsets. In this review, we discuss our current understanding of the role of IL-10 in regulation of immune responses, with a focus on its context-specific roles in intestinal homeostasis, respiratory infection and asthma. We highlight the importance of appropriate production and function of IL-10 for balancing pathogen clearance, control of microbiota and host tissue damage, and that precise modulation of IL-10 functions in vivo could present therapeutic opportunities.
粘膜表面需要错综复杂的免疫调节，以实现对微生物群和无害过敏原的耐受，并防止对病原体的过度炎症反应。细胞因子白细胞介素-10（IL-10）是粘膜免疫调节的关键介质。虽然免疫系统的几乎所有细胞都能产生 IL-10，但它在体内的许多功能取决于调节性或效应 T 细胞群的产生，以及它向巨噬细胞、树突状细胞和特定 T 细胞亚群发出的信号。在这篇综述中，我们将讨论我们目前对 IL-10 在调节免疫反应中的作用的理解，重点是它在肠道稳态、呼吸道感染和哮喘中的特定作用。我们强调了 IL-10 的适当产生和功能对于平衡病原体清除、微生物群控制和宿主组织损伤的重要性，以及在体内精确调节 IL-10 的功能可能带来的治疗机会。
{"title":"Regulation of inflammation by Interleukin-10 in the intestinal and respiratory mucosa","authors":"William J Branchett , Margarida Saraiva , Anne O’Garra","doi":"10.1016/j.coi.2024.102495","DOIUrl":"10.1016/j.coi.2024.102495","url":null,"abstract":"<div><div>Intricate immune regulation is required at mucosal surfaces to allow tolerance to microbiota and harmless allergens and to prevent overexuberant inflammatory responses to pathogens. The cytokine Interleukin-10 (IL-10) is a key mediator of mucosal immune regulation. While IL-10 can be produced by virtually all cells of the immune system, many of its <em>in vivo</em> functions depend upon its production by regulatory or effector T cell populations and its signalling to macrophages, dendritic cells and specific T cell subsets. In this review, we discuss our current understanding of the role of IL-10 in regulation of immune responses, with a focus on its context-specific roles in intestinal homeostasis, respiratory infection and asthma. We highlight the importance of appropriate production and function of IL-10 for balancing pathogen clearance, control of microbiota and host tissue damage, and that precise modulation of IL-10 functions <em>in vivo</em> could present therapeutic opportunities.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142357608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 10.1016/j.coi.2024.102484
Julia C. Johnstone , Yavuz F. Yazicioglu , Alexander J. Clarke
B cells experience extreme alterations in their metabolism throughout their life cycle, from naïve B cells, which have minimal activity, to germinal centre (GC) B cells, which proliferate at the fastest rate of all cells, to long-lived plasma cells with very high levels of protein production that can persist for decades. The underpinning of these transitions remains incompletely understood, and a key question is how utilisation of fuel source supports B cell metabolism. For example, GC B cells, unlike almost all rapidly proliferating cells, mainly use fatty acid oxidation rather than glycolysis. However, following differentiation to plasma cells, their metabolism switches towards a high rate of glucose consumption to aid antibody production. In this review, we discuss the key metabolic pathways in B cells, linking them to cellular signalling events and placing them in the context of disease and therapeutic potential.
B 细胞在其整个生命周期中的新陈代谢都会发生剧烈变化，从活性极低的幼稚 B 细胞，到在所有细胞中增殖速度最快的生殖中心 (GC) B 细胞，再到蛋白质产量极高且可持续数十年之久的长寿命浆细胞。人们对这些转变的基础仍不完全了解，其中一个关键问题是燃料来源的利用如何支持 B 细胞的新陈代谢。例如，GC B 细胞与几乎所有快速增殖的细胞不同，主要利用脂肪酸氧化而不是糖酵解。然而，在分化成浆细胞后，它们的新陈代谢会转向高葡萄糖消耗率，以帮助抗体的产生。在这篇综述中，我们将讨论 B 细胞的关键代谢途径，将它们与细胞信号事件联系起来，并将它们置于疾病和治疗潜力的背景下进行研究。
{"title":"Fuelling B cells: dynamic regulation of B cell metabolism","authors":"Julia C. Johnstone , Yavuz F. Yazicioglu , Alexander J. Clarke","doi":"10.1016/j.coi.2024.102484","DOIUrl":"10.1016/j.coi.2024.102484","url":null,"abstract":"<div><div>B cells experience extreme alterations in their metabolism throughout their life cycle, from naïve B cells, which have minimal activity, to germinal centre (GC) B cells, which proliferate at the fastest rate of all cells, to long-lived plasma cells with very high levels of protein production that can persist for decades. The underpinning of these transitions remains incompletely understood, and a key question is how utilisation of fuel source supports B cell metabolism. For example, GC B cells, unlike almost all rapidly proliferating cells, mainly use fatty acid oxidation rather than glycolysis. However, following differentiation to plasma cells, their metabolism switches towards a high rate of glucose consumption to aid antibody production. In this review, we discuss the key metabolic pathways in B cells, linking them to cellular signalling events and placing them in the context of disease and therapeutic potential.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 10.1016/j.coi.2024.102483
Aydan CH Szeto , Ana CF Ferreira , Andrew NJ McKenzie
T helper 2 (TH2) cells orchestrate type 2 immunity during protective antihelminth immunity and help restore tissue homoeostasis. Their misdirected activities against innocuous substances also underlie atopic diseases, such as asthma and allergy. Recent technological advances are uncovering novel insights into the molecular mechanisms governing TH2 cell differentiation and function.
T 辅助细胞 2（TH2）在保护性抗蠕虫免疫过程中协调 2 型免疫，并帮助恢复组织平衡。它们对无害物质的错误定向活动也是哮喘和过敏等特应性疾病的根源。最近的技术进步正在揭示支配 TH2 细胞分化和功能的分子机制。
{"title":"Molecular mechanisms regulating T helper 2 cell differentiation and function","authors":"Aydan CH Szeto , Ana CF Ferreira , Andrew NJ McKenzie","doi":"10.1016/j.coi.2024.102483","DOIUrl":"10.1016/j.coi.2024.102483","url":null,"abstract":"<div><div>T helper 2 (T<sub>H</sub>2) cells orchestrate type 2 immunity during protective antihelminth immunity and help restore tissue homoeostasis. Their misdirected activities against innocuous substances also underlie atopic diseases, such as asthma and allergy. Recent technological advances are uncovering novel insights into the molecular mechanisms governing T<sub>H</sub>2 cell differentiation and function.</div></div>","PeriodicalId":11361,"journal":{"name":"Current Opinion in Immunology","volume":null,"pages":null},"PeriodicalIF":6.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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