Nature Immunology最新文献_第2页

Astrocyte TRAIL promotes GBM 星形胶质细胞TRAIL促进GBM

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02189-5

Laurie A. Dempsey

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Regulatory T cell therapies to treat autoimmune diseases and transplant rejection 调节性T细胞疗法治疗自身免疫性疾病和移植排斥反应

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02154-2

Jeffrey A. Bluestone, Bruce K. Burnett, Christine E. Crute, Mick D. Fellows, Megan Levings, Hervé Lebrec, Lucilia Pereira Mouriès, Jeffrey Rice, Patricia Rohan, Maria Grazia Roncarolo, Daniel Rotrosen

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Mutated epitopes in SARS-CoV-2 variants are poorly immunogenic SARS-CoV-2变异体中突变的表位免疫原性较差

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02164-0

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Author Correction: Transcription factor Hoxb5 reprograms B cells into functional T lymphocytes 作者更正：转录因子Hoxb5将B细胞重编程为功能性T淋巴细胞

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02181-z

Mengyun Zhang, Yong Dong, Fangxiao Hu, Dan Yang, Qianhao Zhao, Cui Lv, Ying Wang, Chengxiang Xia, Qitong Weng, Xiaofei Liu, Chen Li, Peiqing Zhou, Tongjie Wang, Yuxian Guan, Rongqun Guo, Lijuan Liu, Yang Geng, Hongling Wu, Juan Du, Zheng Hu, Sheng Xu, Jiekai Chen, Aibin He, Bing Liu, Demin Wang, Yong-Guang Yang, Jinyong Wang

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Astrocyte inflammasomes

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02187-7

Ioana Staicu

{"title":"Astrocyte inflammasomes","authors":"Ioana Staicu","doi":"10.1038/s41590-025-02187-7","DOIUrl":"https://doi.org/10.1038/s41590-025-02187-7","url":null,"abstract":"Neuronal synaptic plasticity in the hippocampus is required for the formation of new neuronal connections during memory formation. In Immunity, Zengeler et al. report that inflammasome activation in hippocampus astrocytes regulates hippocampal plasticity, synaptic protein density, neuronal activity, extracellular matrix abundance and IL-33 production. ASC specks and cleaved caspase-1 and IL-18 — but not cleaved IL-1β, cleaved GSDMD or markers of pyroptosis — were detected in GFAP+S100β+ astrocytes, but not IBA1+ microglia, in the hippocampus of healthy mice. Hippocampi from Casp1ΔAst mice had diminished activity and firing and increased density of synaptic markers (VGLUT1 and GABAARα1) in neurons; upregulated memory-related and neurogenesis pathways (with minimal effects on astrocyte transcriptomes); increased production of IL-33 (known to induce engulfment of extracellular matrix to allow synapse rearrangement) in astrocytes and neurons; increased production of the phagolysosome marker CD68 on microglia; and reduced abundance of extracellular matrix. Astrocyte-derived IL-18 restrained the production of IL-33 in neurons. ASC specks and IL-18 expression in the hippocampus were reduced by environmental enrichment and spatial task learning, which suggests that inflammasome activation is integrated in hippocampus physiology.Original reference: Immunity https://doi.org/10.1016/j.immuni.2025.04.007 (2025)","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"51 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201590","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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PD-1 receptor deficiency enhances CD30+ Treg cell function in melanoma PD-1受体缺乏增强黑色素瘤中CD30+ Treg细胞的功能

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02172-0

Jing Xuan Lim, Tegan McTaggart, Seol Kyoung Jung, Katie J. Smith, Gillian Hulme, Stephanie Laba, Yun Qi Ng, Amelia Williams, Rafiqul Hussain, Jonathan Coxhead, Ioana Cosgarea, Catherine Arden, Jérémie Nsengimana, Penny Lovat, Graham Anderson, Hong-Wei Sun, Arian Laurence, Shoba Amarnath

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Tumor lipids suppress NK cells 肿瘤脂质抑制NK细胞

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02186-8

Stephanie Houston

{"title":"Tumor lipids suppress NK cells","authors":"Stephanie Houston","doi":"10.1038/s41590-025-02186-8","DOIUrl":"https://doi.org/10.1038/s41590-025-02186-8","url":null,"abstract":"Patients with peritoneal metastasis can develop ascites, the collection of fluid in the abdomen. Although this has been linked to tumor growth, the mechanisms by which ascites suppresses anti-tumor immunity are unclear. In Science Immunology, Slattery et al. find that natural killer (NK) cells uptake lipids from ascites and this drives NK cell dysfunction, which may contribute to immune suppression in high-grade serous ovarian cancer (HGSOC). In samples from patients with HGSOC, the authors found NK cells in ascites, and these, in addition to NK cells from primary and metastatic tumors, expressed low levels of the activation markers perforin and granzyme B. When NK cells from healthy donors were cultured with ascites from individuals with HGSOC, the tumor killing capacity of NK cells was impaired, the uptake of lipids by NK cells was increased, and there was dysregulation of lipid storage. If lipids were depleted from ascites before culture, NK cell tumor killing capacity was restored. Specifically, phosphatidylcholine (36:1) was present in ascites and accumulated in NK cells, where it caused disruption to the plasma membrane order. The lipid transporter SR-B1 was expressed by NK cells from ascites. If SR-B1 was blocked during culture of ascites and NK cells, there was partial recovery in plasma membrane order, increased expression of cytotoxic molecules and tumor cell killing capacity was improved.Original reference: Sci. Immunol. 10, eadr4795 (2025)","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"11 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201588","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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Succinate undermines FOXP3 stability and disrupts Treg cell function 琥珀酸破坏FOXP3的稳定性，破坏Treg细胞的功能

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02167-x

Ye Zheng

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Succinate drives gut inflammation by promoting FOXP3 degradation through a molecular switch 琥珀酸盐通过分子开关促进FOXP3降解，从而引发肠道炎症

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-06-02 DOI: 10.1038/s41590-025-02166-y

Hai Wang, Danqing Hu, Yang Cheng, Qiong Gao, Kun Liu, Nikita L. Mani, Amy Y. Tang, Radhika Iyer, Beixue Gao, Leyu Sun, Qi Zhou, Qin Yu, Samuel E. Weinberg, Xiaoyu Zhang, Yingzi Cong, Parambir S. Dulai, Yana Zhang, Zheng Liu, Deyu Fang

{"title":"Succinate drives gut inflammation by promoting FOXP3 degradation through a molecular switch","authors":"Hai Wang, Danqing Hu, Yang Cheng, Qiong Gao, Kun Liu, Nikita L. Mani, Amy Y. Tang, Radhika Iyer, Beixue Gao, Leyu Sun, Qi Zhou, Qin Yu, Samuel E. Weinberg, Xiaoyu Zhang, Yingzi Cong, Parambir S. Dulai, Yana Zhang, Zheng Liu, Deyu Fang","doi":"10.1038/s41590-025-02166-y","DOIUrl":"https://doi.org/10.1038/s41590-025-02166-y","url":null,"abstract":"Succinate levels are increased in inflammatory bowel disease (IBD), but its role in disease pathogenicity remains unknown. Here we showed that succinate promoted colitis in mice by reducing the expression of FOXP3 and increasing the expression of interleukin-17 in regulatory T (Treg) cells. Succinate selectively reduced the expression of 2-oxoglutarate dehydrogenase complex (OGDHc), the enzyme for succinyl-CoA synthesis, which in turn reduced FOXP3 succinylation and made FOXP3 lysine residues available for ubiquitination and FOXP3 protein degradation. Genetic deletion of Dlst, a member of OGDHc, in Treg cells led to reduced expression of FOXP3, impaired Treg cells function and severe gut inflammation. Restoring FOXP3 expression fully rescued the immune suppressive functions of Dlst-deficient Treg cells. In individuals with IBD, FOXP3 and OGDHc levels were reduced in Treg cells and negatively correlated with succinate levels and inflammation severity. This study identifies succinate as a pathogenic factor in IBD, uncovering a succinate-driven molecular switch that regulates FOXP3 stability and Treg cells function during inflammation.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"13 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144201594","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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The IL-22–oncostatin M axis promotes intestinal inflammation and tumorigenesis il -22抑制素M轴促进肠道炎症和肿瘤发生

IF 30.5 1区医学

Nature Immunology Pub Date : 2025-05-30 DOI: 10.1038/s41590-025-02149-z

Roodline Cineus, Yanjiang Luo, Mariia Saliutina, Subhakankha Manna, Camila A. Cancino, Luis Velasco Blázquez, Lifen Wang, Diana Bösel, Aya Abdelrahman, Joanna E. Klementowicz, Alexis Scherl, Saskia Hainbuch, Béatrice Bréart, Gino Kwon, Agata Konopka, Gabriela M. Guerra, Elena von Coburg, Lorenz Gerbeth, Juliette Roels, Frederik Heinrich, Nils Müller, Pawel Durek, Nikolaus Deigendesch, James Ziai, Jeffrey Hung, Thomas Conrad, Anja A. Kühl, Stefan Wirtz, Max Löhning, Mary Keir, Andreas Diefenbach, Mir-Farzin Mashreghi, Britta Siegmund, Michael Schumann, Chiara Romagnani, Nathaniel R. West, Ahmed N. Hegazy

{"title":"The IL-22–oncostatin M axis promotes intestinal inflammation and tumorigenesis","authors":"Roodline Cineus, Yanjiang Luo, Mariia Saliutina, Subhakankha Manna, Camila A. Cancino, Luis Velasco Blázquez, Lifen Wang, Diana Bösel, Aya Abdelrahman, Joanna E. Klementowicz, Alexis Scherl, Saskia Hainbuch, Béatrice Bréart, Gino Kwon, Agata Konopka, Gabriela M. Guerra, Elena von Coburg, Lorenz Gerbeth, Juliette Roels, Frederik Heinrich, Nils Müller, Pawel Durek, Nikolaus Deigendesch, James Ziai, Jeffrey Hung, Thomas Conrad, Anja A. Kühl, Stefan Wirtz, Max Löhning, Mary Keir, Andreas Diefenbach, Mir-Farzin Mashreghi, Britta Siegmund, Michael Schumann, Chiara Romagnani, Nathaniel R. West, Ahmed N. Hegazy","doi":"10.1038/s41590-025-02149-z","DOIUrl":"https://doi.org/10.1038/s41590-025-02149-z","url":null,"abstract":"Multicellular cytokine networks drive intestinal inflammation and colitis-associated cancer (CAC). Interleukin-22 (IL-22) exerts both protective and pathogenic effects in the intestine, but the mechanisms that regulate this balance remain unclear. Here, we identify that IL-22 directly induces responsiveness to the IL-6 family cytokine oncostatin M (OSM) in intestinal epithelial cells (IECs) by activating STAT3 and upregulating the OSM receptor. In turn, OSM synergizes with IL-22 to sustain STAT3 activation in IECs and promote proinflammatory epithelial adaptation and immune cell chemotaxis to the inflamed intestine. Conditional deletion of the OSM receptor in IECs protects mice from both colitis and CAC, and pharmacological blockade of OSM attenuates established CAC. Thus, IL-22 and OSM form a pathogenic circuit that drives inflammation and tumorigenesis. Our findings reveal a previously unknown mechanism by which OSM supports intestinal pathology and highlight the IL-22–OSM axis as a promising therapeutic target for inflammatory bowel disease and CAC.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"36 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176648","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