Nature Immunology最新文献

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Monocyte-derived macrophages are too much of a good thing in lung fibrosis 单核细胞衍生的巨噬细胞在肺纤维化中是个太好的东西
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-04 DOI: 10.1038/s41590-024-01989-5
Leif Erik Sander
{"title":"Monocyte-derived macrophages are too much of a good thing in lung fibrosis","authors":"Leif Erik Sander","doi":"10.1038/s41590-024-01989-5","DOIUrl":"https://doi.org/10.1038/s41590-024-01989-5","url":null,"abstract":"Acute lung injury elicits a profibrotic wound healing program in monocyte-derived macrophages. Their abundance is associated with pulmonary fibrosis in individuals recovering from COVID-19 pneumonia.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370044","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}
引用次数: 0
DNA-sensing pathways in health, autoinflammatory and autoimmune diseases 健康、自身炎症和自身免疫疾病中的 DNA 传感途径
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-04 DOI: 10.1038/s41590-024-01966-y
Mingqi Dong, Katherine A. Fitzgerald
{"title":"DNA-sensing pathways in health, autoinflammatory and autoimmune diseases","authors":"Mingqi Dong, Katherine A. Fitzgerald","doi":"10.1038/s41590-024-01966-y","DOIUrl":"https://doi.org/10.1038/s41590-024-01966-y","url":null,"abstract":"<p>Detection of microbial DNA is a primary means of host defense. In mammalian cells, DNA-sensing pathways induce robust anti-microbial responses and initiation of adaptive immunity, leading to the eventual clearance of the infectious agent. However, while conferring the advantage of broad detection capability, the sequence-independent recognition mechanisms of most DNA sensors pose a significant challenge for mammalian cells to maintain ignorance to self-DNA under homeostatic conditions. In this Review, we summarize the fundamentals of DNA-sensing pathways and the intricate regulatory networks that keep these pathways in check. In addition, we describe how regulatory restraints can be defective and underlie human autoinflammatory and autoimmune diseases. Further, we discuss therapies in development that limit inflammation fueled by self-DNA or inappropriate activation of DNA-sensing pathways.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370048","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}
引用次数: 0
Profibrotic monocyte-derived alveolar macrophages are expanded in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19 在 COVID-19 后出现持续呼吸道症状和放射学异常的患者中,肺泡巨噬细胞源性增殖性单核细胞扩增
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-04 DOI: 10.1038/s41590-024-01975-x
Joseph I. Bailey, Connor H. Puritz, Karolina J. Senkow, Nikolay S. Markov, Estefani Diaz, Emmy Jonasson, Zhan Yu, Suchitra Swaminathan, Ziyan Lu, Samuel Fenske, Rogan A. Grant, Hiam Abdala-Valencia, Ruben J. Mylvaganam, Amy Ludwig, Janet Miller, R. Ian Cumming, Robert M. Tighe, Kymberly M. Gowdy, Ravi Kalhan, Manu Jain, Ankit Bharat, Chitaru Kurihara, Ruben San Jose Estepar, Raul San Jose Estepar, George R. Washko, Ali Shilatifard, Jacob I. Sznajder, Karen M. Ridge, G. R. Scott Budinger, Rosemary Braun, Alexander V. Misharin, Marc A. Sala
{"title":"Profibrotic monocyte-derived alveolar macrophages are expanded in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19","authors":"Joseph I. Bailey, Connor H. Puritz, Karolina J. Senkow, Nikolay S. Markov, Estefani Diaz, Emmy Jonasson, Zhan Yu, Suchitra Swaminathan, Ziyan Lu, Samuel Fenske, Rogan A. Grant, Hiam Abdala-Valencia, Ruben J. Mylvaganam, Amy Ludwig, Janet Miller, R. Ian Cumming, Robert M. Tighe, Kymberly M. Gowdy, Ravi Kalhan, Manu Jain, Ankit Bharat, Chitaru Kurihara, Ruben San Jose Estepar, Raul San Jose Estepar, George R. Washko, Ali Shilatifard, Jacob I. Sznajder, Karen M. Ridge, G. R. Scott Budinger, Rosemary Braun, Alexander V. Misharin, Marc A. Sala","doi":"10.1038/s41590-024-01975-x","DOIUrl":"https://doi.org/10.1038/s41590-024-01975-x","url":null,"abstract":"<p>Monocyte-derived alveolar macrophages drive lung injury and fibrosis in murine models and are associated with pulmonary fibrosis in humans. Monocyte-derived alveolar macrophages have been suggested to develop a phenotype that promotes lung repair as injury resolves. We compared single-cell and cytokine profiling of the alveolar space in a cohort of 35 patients with post-acute sequelae of COVID-19 who had persistent respiratory symptoms and abnormalities on a computed tomography scan of the chest that subsequently improved or progressed. The abundance of monocyte-derived alveolar macrophages, their gene expression programs, and the level of the monocyte chemokine CCL2 in bronchoalveolar lavage fluid positively associated with the severity of radiographic fibrosis. Monocyte-derived alveolar macrophages from patients with resolving or progressive fibrosis expressed the same set of profibrotic genes. Our findings argue against a distinct reparative phenotype in monocyte-derived alveolar macrophages, highlighting their utility as a biomarker of failed lung repair and a potential target for therapy.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370046","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}
引用次数: 0
AI and immunology as a new research paradigm 人工智能和免疫学是一种新的研究范式
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-04 DOI: 10.1038/s41590-024-01974-y
Anupama E. Gururaj, Richard H. Scheuermann, Dawei Lin
{"title":"AI and immunology as a new research paradigm","authors":"Anupama E. Gururaj, Richard H. Scheuermann, Dawei Lin","doi":"10.1038/s41590-024-01974-y","DOIUrl":"https://doi.org/10.1038/s41590-024-01974-y","url":null,"abstract":"The National Institute of Allergy and Infectious Diseases (NIAID) hosted a symposium on ‘AI and Immunology: Exploring Challenges and Opportunities’. The event considered how artificial intelligence (AI) can advance research on the multi-scale, adaptive immune system to improve human health, covering basic research and clinical use cases, data and AI model fundamentals.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370045","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}
引用次数: 0
GPR34 is a metabolic immune checkpoint for ILC1-mediated antitumor immunity GPR34 是 ILC1 介导的抗肿瘤免疫的代谢免疫检查点
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-02 DOI: 10.1038/s41590-024-01973-z
Jiaxian Yan, Chi Zhang, Yueli Xu, Zonghui Huang, Qingyuan Ye, Xiaojun Qian, Liang Zhu, Guangming Huang, Xiaqiong Wang, Wei Jiang, Rongbin Zhou
{"title":"GPR34 is a metabolic immune checkpoint for ILC1-mediated antitumor immunity","authors":"Jiaxian Yan, Chi Zhang, Yueli Xu, Zonghui Huang, Qingyuan Ye, Xiaojun Qian, Liang Zhu, Guangming Huang, Xiaqiong Wang, Wei Jiang, Rongbin Zhou","doi":"10.1038/s41590-024-01973-z","DOIUrl":"https://doi.org/10.1038/s41590-024-01973-z","url":null,"abstract":"<p>Type 1 innate lymphoid cells (ILC1s) are a class of tissue-resident cells with antitumor activity, suggesting its possible role in solid tumor immune surveillance, but it is not clear whether manipulating ILC1s can induce potent antitumor immune responses. Here, we found that G-protein-coupled receptor 34 (GPR34), a receptor for lysophosphatidylserine (LysoPS), was highly expressed on ILC1s but not on conventional natural killer cells in the tumor microenvironment. LysoPS was enriched in the tumor microenvironment and could inhibit ILC1 activation via GPR34. Genetic deletion of LysoPS synthase <i>Abhd16a</i> expression in tumors or <i>Gpr34</i> expression in ILC1s or antagonizing GPR34 enhanced ILC1 antitumor activity. In individuals with cancer, <i>ABHD16A</i> expression in tumors or <i>GPR34</i> expression in ILC1s was inversely correlated with the antitumor activity of ILC1s or ILC1-like cells. Thus, our results demonstrate that manipulating ILC1s can induce potent antitumor immunity, and GPR34 is a metabolic immune checkpoint that can be targeted to develop ILC1-based immunotherapy.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142362777","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}
引用次数: 0
Author Correction: Immunological imprinting and risks of influenza B virus infection 作者更正:免疫印记与感染乙型流感病毒的风险
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-02 DOI: 10.1038/s41590-024-01996-6
Isaac C. L. Chow, Sook-San Wong
{"title":"Author Correction: Immunological imprinting and risks of influenza B virus infection","authors":"Isaac C. L. Chow, Sook-San Wong","doi":"10.1038/s41590-024-01996-6","DOIUrl":"https://doi.org/10.1038/s41590-024-01996-6","url":null,"abstract":"<p>Correction to: <i>Nature Immunology</i> https://doi.org/10.1038/s41590-024-01906-w, published online 19 July 2024.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363101","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}
引用次数: 0
MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33 MrgprA3神经元通过选择性控制髓源性IL-33驱动皮肤对蠕虫的免疫力
IF 30.5 1区 医学
Nature Immunology Pub Date : 2024-10-01 DOI: 10.1038/s41590-024-01982-y
Juan M. Inclan-Rico, Camila M. Napuri, Cailu Lin, Li-Yin Hung, Annabel A. Ferguson, Xiaohong Liu, Qinxue Wu, Christopher F. Pastore, Adriana Stephenson, Ulrich M. Femoe, Fungai Musaigwa, Heather L. Rossi, Bruce D. Freedman, Danielle R. Reed, Tomáš Macháček, Petr Horák, Ishmail Abdus-Saboor, Wenqin Luo, De’Broski R. Herbert
{"title":"MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33","authors":"Juan M. Inclan-Rico, Camila M. Napuri, Cailu Lin, Li-Yin Hung, Annabel A. Ferguson, Xiaohong Liu, Qinxue Wu, Christopher F. Pastore, Adriana Stephenson, Ulrich M. Femoe, Fungai Musaigwa, Heather L. Rossi, Bruce D. Freedman, Danielle R. Reed, Tomáš Macháček, Petr Horák, Ishmail Abdus-Saboor, Wenqin Luo, De’Broski R. Herbert","doi":"10.1038/s41590-024-01982-y","DOIUrl":"https://doi.org/10.1038/s41590-024-01982-y","url":null,"abstract":"<p>Skin uses interdependent cellular networks for barrier integrity and host immunity, but most underlying mechanisms remain obscure. Herein, we demonstrate that the human parasitic helminth <i>Schistosoma mansoni</i> inhibited pruritus evoked by itch-sensing afferents bearing the Mas-related G-protein-coupled receptor A3 (MrgprA3) in mice. MrgprA3 neurons controlled interleukin (IL)-17<sup>+</sup> γδ T cell expansion, epidermal hyperplasia and host resistance against <i>S. mansoni</i> through shaping cytokine expression in cutaneous antigen-presenting cells. MrgprA3 neuron activation downregulated IL-33 but induced IL-1β and tumor necrosis factor in macrophages and type 2 conventional dendritic cells partially through the neuropeptide calcitonin gene-related peptide. Macrophages exposed to MrgprA3-derived secretions or bearing cell-intrinsic IL-33 deletion showed increased chromatin accessibility at multiple inflammatory cytokine loci, promoting IL-17/IL-23-dependent changes to the epidermis and anti-helminth resistance. This study reveals a previously unrecognized intercellular communication mechanism wherein itch-inducing MrgprA3 neurons initiate host immunity against skin-invasive parasites by directing cytokine expression patterns in myeloid antigen-presenting cell subsets.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":30.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142330433","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}
引用次数: 0
Inflammatory blood clots 炎性血凝块
IF 27.7 1区 医学
Nature Immunology Pub Date : 2024-09-27 DOI: 10.1038/s41590-024-01980-0
Ioana Staicu
{"title":"Inflammatory blood clots","authors":"Ioana Staicu","doi":"10.1038/s41590-024-01980-0","DOIUrl":"10.1038/s41590-024-01980-0","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":27.7,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328579","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}
引用次数: 0
Old and new mpox vaccine 新旧麻疹疫苗
IF 27.7 1区 医学
Nature Immunology Pub Date : 2024-09-27 DOI: 10.1038/s41590-024-01979-7
Paula Jauregui
{"title":"Old and new mpox vaccine","authors":"Paula Jauregui","doi":"10.1038/s41590-024-01979-7","DOIUrl":"10.1038/s41590-024-01979-7","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":27.7,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328549","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}
引用次数: 0
Editing cancer in vivo 体内编辑癌症
IF 27.7 1区 医学
Nature Immunology Pub Date : 2024-09-27 DOI: 10.1038/s41590-024-01978-8
Nicholas J. Bernard
{"title":"Editing cancer in vivo","authors":"Nicholas J. Bernard","doi":"10.1038/s41590-024-01978-8","DOIUrl":"10.1038/s41590-024-01978-8","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":null,"pages":null},"PeriodicalIF":27.7,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328587","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}
引用次数: 0
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