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Structures of butyrophilin multimers reveal a plier-like mechanism for Vγ9Vδ2 T cell receptor activation 亲丁酸蛋白多聚体的结构揭示了v - γ - 9v - δ2 T细胞受体激活的钳状机制
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-11 DOI: 10.1016/j.immuni.2025.05.011
Mai Zhang, Yiqing Wang, Ningning Cai, Yingying Qu, Xianqiang Ma, Jing Xue, Xiaorui Chen, Xueguang Zhang, Junyu Xiao, Yonghui Zhang
{"title":"Structures of butyrophilin multimers reveal a plier-like mechanism for Vγ9Vδ2 T cell receptor activation","authors":"Mai Zhang, Yiqing Wang, Ningning Cai, Yingying Qu, Xianqiang Ma, Jing Xue, Xiaorui Chen, Xueguang Zhang, Junyu Xiao, Yonghui Zhang","doi":"10.1016/j.immuni.2025.05.011","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.011","url":null,"abstract":"Vγ9Vδ2 T cells, the major circulating human γδ T cell subset, respond to infections and tumors by recognizing phosphoantigens (pAgs) via transmembrane butyrophilins (BTN3A1, BTN3A2, and BTN2A1). Here, using cryoelectron microscopy, we resolved the structures of BTN multimers bound to the microbial pAg HMBPP alone and in complex with the T cell receptor (TCR). These structures reveal that BTN3A1 and BTN2A1 cooperate to sense pAgs through their intracellular B30.2 domains, whereas BTN3A2 and BTN2A1 interact extracellularly. TCR engagement triggers its conformational changes, allowing BTN2A1 to bind the Vγ9 chain laterally and BTN3A2 to interact apically with the Vδ2 chain’s germline-encoded regions and CDR3 motif, as well as the Vγ9 CDR3. Our study uncovers a “plier-like gripping” mechanism, where BTN multimers bridge the TCR surface to drive activation. These findings establish a structural foundation for γδ T cell-targeted immunotherapies distinct from αβ T cell strategies reliant on major-histocompatibility-complex-mediated antigen presentation.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"9 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144260303","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
An inside job—CHIP infiltrates and promotes cancer 一个内部的job-CHIP渗透并促进癌症
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.014
Brian Y. Soong, Nader Yatim, Miriam Merad
{"title":"An inside job—CHIP infiltrates and promotes cancer","authors":"Brian Y. Soong, Nader Yatim, Miriam Merad","doi":"10.1016/j.immuni.2025.05.014","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.014","url":null,"abstract":"Somatic mutations in hematopoietic stem cells can lead to clonal hematopoiesis of indeterminate potential (CHIP), a frequent condition associated with many age-related diseases including solid cancer. In the <em>New England Journal of Medicine</em>, Pich et al. report that tumor-infiltrating CHIP correlates with worsened cancer prognosis and clinical outcomes, providing evidence for the impact of mutated immune cells on disease progression.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"50 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252437","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
A backhanded complement: Prostacyclin turns inflammation off from the inside out 一个反唇相讥的补充：前列环素可以从内到外消除炎症
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.009
Samuel E.J. Preston, Russell G. Jones
{"title":"A backhanded complement: Prostacyclin turns inflammation off from the inside out","authors":"Samuel E.J. Preston, Russell G. Jones","doi":"10.1016/j.immuni.2025.05.009","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.009","url":null,"abstract":"To limit hyperactive T helper (Th)1-driven pathology, it is crucial that this T cell population contracts upon pathogen clearance. In this issue of <em>Immunity</em>, Rahman et al. define a complement-C5-mediated lipid-class-switch mechanism that regulates Th1 self-control. Following activation, enhanced cell-intrinsic prostacyclin (PGI<sub>2</sub>) signaling boosts interleukin (IL)-1R2 production to facilitate Th1 cell contraction.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"814 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252674","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
Evolutionary medicine in action: Sickle hemoglobin fuels tumor progression 进化医学的作用：镰状血红蛋白促进肿瘤进展
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.012
Miguel P. Soares
{"title":"Evolutionary medicine in action: Sickle hemoglobin fuels tumor progression","authors":"Miguel P. Soares","doi":"10.1016/j.immuni.2025.05.012","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.012","url":null,"abstract":"Evolutionary medicine integrates principles of evolutionary biology to understand and treat human diseases. As a classical example, positive selection of the sickle hemoglobin mutation, which confers a survival advantage against malaria in heterozygous individuals, causes sickle cell disease in homozygotes. In this issue of <em>Immunity</em>, Zilong Zhao et al. report a possible additional evolutionary trade-off associated with sickle hemoglobin: compromised anti-tumor immunity.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"40 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252668","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
Mamma MIA! Decidual NK cells involved in fetal neurodevelopment 《妈妈咪呀!》蜕膜NK细胞参与胎儿神经发育
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.010
Norman Shreeve, Francesco Colucci
{"title":"Mamma MIA! Decidual NK cells involved in fetal neurodevelopment","authors":"Norman Shreeve, Francesco Colucci","doi":"10.1016/j.immuni.2025.05.010","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.010","url":null,"abstract":"Maternal immune activation (MIA) can cause neurodevelopmental disorders, but the underlying mechanisms are incompletely understood. In this issue of <em>Immunity</em>, Bian et al. show that MIA triggers decidual NK cells to secrete granzyme B, which crosses the placenta and disturbs microglial homeostasis in the fetal brain, leading to abnormal neurodevelopment.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"7 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252704","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
Spectosis: Dying for a complement Spectosis：渴望补充
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.017
Jared R. Coombs, Sabrina S. Burgener, Kate Schroder
{"title":"Spectosis: Dying for a complement","authors":"Jared R. Coombs, Sabrina S. Burgener, Kate Schroder","doi":"10.1016/j.immuni.2025.05.017","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.017","url":null,"abstract":"Red blood cells (RBCs) undergo pathological cell death in hemolytic diseases. In a recent issue of <em>Cell</em>, Chen et al. reveal a mode of programmed cell death, spectosis, in which complement activation initiates (mini)NLRP3-caspase-8 complexes, culminating in hemolysis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"88 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252438","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
Cytotoxic IgG: Mechanisms, functions, and applications 细胞毒性IgG：机制、功能和应用
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.008
Miriam Wöhner, Falk Nimmerjahn
{"title":"Cytotoxic IgG: Mechanisms, functions, and applications","authors":"Miriam Wöhner, Falk Nimmerjahn","doi":"10.1016/j.immuni.2025.05.008","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.008","url":null,"abstract":"A key feature of immunoglobulin G (IgG) antibodies is their capacity to deplete target cells, which is broadly referred to as antibody-dependent cellular cytotoxicity (ADCC). The capacity to kill target cells has made cytotoxic antibodies the standard of care for many malignant, autoimmune, and infectious diseases. However, cytotoxic antibody activity in therapeutic settings is often limited, and current optimization approaches have only mildly enhanced therapeutic efficacy. In this review, we discuss the highly complex molecular and cellular pathways underlying an ADCC reaction and how these are impacted by the type of target cell, the effector cells, and the tissue environment. We also discuss implications for improving therapies and provide an updated model of cytotoxic IgG activity.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"40 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252675","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
A sweet spot in myeloid cell pro-tumoral functions 骨髓细胞促肿瘤功能的最佳点
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-10 DOI: 10.1016/j.immuni.2025.05.015
Gillian Dunphy, David Sancho
{"title":"A sweet spot in myeloid cell pro-tumoral functions","authors":"Gillian Dunphy, David Sancho","doi":"10.1016/j.immuni.2025.05.015","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.015","url":null,"abstract":"The regulation of myeloid cell responses can determine tumor outcomes. In this issue of <em>Immunity</em>, Blidner et al. report that galectin-1 triggers both immunoregulatory and pro-angiogenic circuits in myeloid cells, promoting tumor growth via a VEGF-dependent mechanism.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"215 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144252669","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
Dectin-1 facilitates lung fungal-mediated pulmonary fibrosis Dectin-1促进肺真菌介导的肺纤维化
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-09 DOI: 10.1016/j.immuni.2025.05.007
Ding Qiu, Shuishen Zhang, Chanyan Huang, Xinying Wang, Jianping Deng, Haiyang Sun, Bingbing Feng, Ying Tan, Kaile Ji, Shaoting Xu, Xiaoqi Ye, Chao Cheng, Shigeru Kakuta, Yoshiyuki Adachi, Yoichiro Iwakura, Shuai Wang, Shaowei Dong, Ce Tang
{"title":"Dectin-1 facilitates lung fungal-mediated pulmonary fibrosis","authors":"Ding Qiu, Shuishen Zhang, Chanyan Huang, Xinying Wang, Jianping Deng, Haiyang Sun, Bingbing Feng, Ying Tan, Kaile Ji, Shaoting Xu, Xiaoqi Ye, Chao Cheng, Shigeru Kakuta, Yoshiyuki Adachi, Yoichiro Iwakura, Shuai Wang, Shaowei Dong, Ce Tang","doi":"10.1016/j.immuni.2025.05.007","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.007","url":null,"abstract":"Dectin-1 (<em>Clec7a</em>), a C-type lectin receptor for β-glucans, is critical in host defense against fungal infections and has been implicated in allergic responses, yet its role in pulmonary fibrosis remains unclear. In this study, we reveal that bleomycin-induced pulmonary fibrosis was suppressed in Dectin-1-deficient mice, mediated by interactions with the commensal lung fungus <em>Engyodontium</em>. Dectin-1 was predominantly expressed on alveolar macrophages (AMs), correlating with fibrosis severity in both humans and mice. Dectin-1 deficiency reduced Arginase-1 and TGF-β-producing AMs and profibrotic factor expression. Mechanistically, Dectin-1 signaling promoted quiescent AM differentiation into profibrotic AMs via the Raf1-dependent pathway, bypassing CARD9 signaling and mono-macrophage chemotactic recruitment. Therapeutic targeting of Dectin-1 with laminarin or Raf1 inhibitors attenuated fibrosis in mice and reduced profibrotic factors in human AMs and fibroblasts. These findings highlight the Dectin-1-Raf1 axis as a key regulator of pulmonary fibrosis and a promising therapeutic target for fibrotic diseases.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"16 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144237995","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
Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair 组织修复需要空间限制和不同的肝巨噬细胞
IF 32.4 1区 医学
Immunity Pub Date : 2025-06-06 DOI: 10.1016/j.immuni.2025.05.013
{"title":"Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair","authors":"","doi":"10.1016/j.immuni.2025.05.013","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.013","url":null,"abstract":"No Abstract","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"39 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228852","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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