Nature Immunology最新文献

{"title":"Author Correction: Mapping self-associating chromatin hubs identifies Id proteins as key determinants of exhausted CD8+ T cell fate","authors":"Wei Hu,Qing Chen,Shaoqi Zhu,Shengen Shawn Hu,Haibo Yu,Vanita Patel,Ying Wang,Vladimir P. Badovinac,Yi Zhang,Chongzhi Zang,Weiqun Peng,Hai-Hui Xue","doi":"10.1038/s41590-026-02695-0","DOIUrl":"https://doi.org/10.1038/s41590-026-02695-0","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"2 3-4 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149021322","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}

{"title":"Author Correction: Exhausted CD8+ T cell fate is programmed by dynamic CTCF-mediated enhancer activation and invariant CTCF-imposed barriers","authors":"Wei Hu,Shaoqi Zhu,Qing Chen,Vladimir P. Badovinac,Weiqun Peng,Hai-Hui Xue","doi":"10.1038/s41590-026-02694-1","DOIUrl":"https://doi.org/10.1038/s41590-026-02694-1","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"65 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149022464","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}

{"title":"Metastasis enables immunogenicity through migrasome-mediated antigen release","authors":"Dong Jiang, Jinzhao He, Renxiang Xie, Minghui Shi, Siyuan Liu, Haohao Jia, Bingjie Yang, Xiaojie Ruan, Xiaoyu Tao, Yuhan Xiang, Yining Chen, Lin Jiao, Xiaoyu Feng, Li Yu","doi":"10.1038/s41590-026-02641-0","DOIUrl":"10.1038/s41590-026-02641-0","url":null,"abstract":"Antigen release is a critical step in initiating antitumor immune responses, yet its regulation during metastasis is not well understood. Here we show that circulating tumor cells undergoing vascular migration produce migrasomes that serve as a metastasis-specific mechanism of antigen release. These migrasomes are enriched in tumor-associated antigens, including cancer-testis and mutated antigens, and are captured efficiently by antigen-presenting cells in secondary lymphoid organs, where they undergo cross-presentation to elicit CD8+ T cell-mediated immune responses that constrain metastatic progression. Genetic inhibition of migrasome formation enhances metastasis, while administration of purified cancer-derived migrasomes restores immune-mediated suppression of metastatic growth. These findings show paradoxically that metastasis can enhance tumor immunogenicity through migrasome-mediated antigen release, highlighting a link between cancer dissemination and immune activation and establishing migrasomes as a distinct and potent platform for endogenous tumor antigen delivery. Here the authors show that circulating tumor cells shed migrasomes that carry tumor antigens, which in turn can activate CD8+ T cells through cross-presentation to restrict metastasis.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"2088-2101"},"PeriodicalIF":26.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02641-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149021323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Updating the symbols of ten cytokines and their receptors: report of the IUIS Cytokine Nomenclature Sub-Committee","authors":"Diana Boraschi,Chen Dong,Humberto Lanz-Mendoza,Lazaro Moreira Marques-Neto,Nima Rezaei,Elspeth Bruford","doi":"10.1038/s41590-026-02654-9","DOIUrl":"https://doi.org/10.1038/s41590-026-02654-9","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"7 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149021325","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}

{"title":"Author Correction: Non-catalytic ubiquitin binding by A20 prevents psoriatic arthritis–like disease and inflammation","authors":"Bahram Razani,Michael I. Whang,Francis S. Kim,Mary C. Nakamura,Xiaofei Sun,Rommel Advincula,Jessie A. Turnbaugh,Mihir Pendse,Priscilia Tanbun,Philip Achacoso,Peter J. Turnbaugh,Barbara A. Malynn,Averil Ma","doi":"10.1038/s41590-026-02687-0","DOIUrl":"https://doi.org/10.1038/s41590-026-02687-0","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"9 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149021324","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}

{"title":"Deletion of a distal IRF4 element prevents inflammation-induced reprogramming of human regulatory T cell fate","authors":"Patrick Ho, Alexander Vu, Joey Leung, Wendy Rosenthal, Vasilis Ntranos, Jeffrey A. Bluestone, Qizhi Tang","doi":"10.1038/s41590-026-02655-8","DOIUrl":"10.1038/s41590-026-02655-8","url":null,"abstract":"Regulatory T (Treg) cells in mice can lose lineage identity and acquire proinflammatory functions, but whether human Treg cells are similarly susceptible to cytokine-driven destabilization remains unclear. Here we established an in vitro model of human Treg cell destabilization defined by silencing of the lineage-specifying transcription factor FOXP3, loss of suppressive function and acquisition of proinflammatory activity. Single-cell chromatin accessibility and transcriptomic profiling revealed a genome-wide increase in accessibility at AP-1-binding sites, including a putative regulatory element distal to IRF4. Increased accessibility at this element correlated with increased IRF4 expression during Treg cell destabilization, and its excision conferred resistance to inflammatory cytokine-induced reprogramming. Conversely, forced expression of IRF4 together with BATF promoted Treg cell destabilization. These data identify a distal IRF4 regulatory element as a critical node enabling heightened AP-1-IRF4 cooperative activity to drive Treg cell destabilization, with implications for the design of more stable and effective Treg cell-based therapies. Tang and colleagues identify a distal IRF4 chromatin regulatory region that governs human Treg cell stability.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"2143-2155"},"PeriodicalIF":26.5,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02655-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149010502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal single-cell profiling reveals T cell clonal dynamics and phenotypic plasticity in human graft-versus-host disease","authors":"Lingting Shi, Ajna Uzuni, Ximi K. Wang, Michael Pressler, David W. Harle, Shami Chakrabarti, Rodney Macedo, Kirubel Belay, Christian A. Gordillo, Thomas McMahon-Skates, Erik Raps, Jia Yi Ady Zhang, Achille Nazaret, Joy L. Fan, Yinuo Jin, Xumin Shen, Joshua S. Fuller, Tamjeed Azad, Jessie Huang, Pranik Chainani, Jose Pomarino Nima, Julian A. Abrams, Armando Del Portillo, Markus Y. Mapara, Mohamed Alhamar, Megan Sykes, José L. McFaline-Figueroa, Elham Azizi, Ran Reshef","doi":"10.1038/s41590-026-02631-2","DOIUrl":"10.1038/s41590-026-02631-2","url":null,"abstract":"Allogeneic hematopoietic cell transplantation cures hematologic diseases but is limited by acute graft‑versus‑host disease. How human T cell clones drive epithelial injury remains poorly mapped. We studied 31 transplant recipients, integrating longitudinal T cell antigen receptor (TCR) profiling with single-cell RNA sequencing/TCR sequencing and spatial transcriptomics to track T cell clonal dynamics. We developed DecompTCR to resolve temporal dynamics and adapted computational tools to map clone phenotypes and niches in tissue. Our analyses revealed that cyclophosphamide selectively depletes alloreactive clones, although insufficient early expansion leads to incomplete depletion and severe disease. Severe graft‑versus‑host disease is marked by persistent expansion of alloreactive clones, rewiring of homeostatic cell types and diversification of donor-derived CD8+ clonotypes that acquire Hobit (ZNF683)+ tissue‑resident memory T (TRM) cell programs during migration to epithelium. Spatial deconvolution identified CD8+ effector/Hobit+ TRM hubs near intestinal stem‑cell-rich crypt bases and crypt‑loss regions. This clonotype‑resolved framework links tissue‑instructed TRM cell remodeling to localized epithelial injury, nominating early-repertoire dynamics and spatial hub burden as biomarkers. Shi et al. use a spatiotemporal framework to profile alloreactive T cells in humans undergoing hematopoietic cell transplantation and demonstrate how severe graft‑versus‑host disease is driven by tissue-resident memory programs that target intestinal stem cell niches.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"2156-2171"},"PeriodicalIF":26.5,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990728","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}

{"title":"Author Correction: The transcription factor TCF-1 initiates the differentiation of T_FH cells during acute viral infection.","authors":"Lifan Xu, Yi Cao, Zhunyi Xie, Qizhao Huang, Qiang Bai, Xia Yang, Ran He, Yaxing Hao, Haoqiang Wang, Tingting Zhao, Zhonglei Fan, Aijian Qin, Jianqiang Ye, Xinyuan Zhou, Lilin Ye, Yuzhang Wu","doi":"10.1038/s41590-026-02681-6","DOIUrl":"https://doi.org/10.1038/s41590-026-02681-6","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":" ","pages":""},"PeriodicalIF":26.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148983219","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}

{"title":"ANKRD11 deficiency reprograms CD8+ T cell differentiation to enhance immunity in chronic infection and cancer","authors":"Wei Xu, Jie Guo, Xue Cao, Liping Li, Pei Xiao, Xinchao Zhang, Qiuzhu Jin, Fuping Zhang, Baidong Hou, Minghui Li, Xuyu Zhou","doi":"10.1038/s41590-026-02652-x","DOIUrl":"10.1038/s41590-026-02652-x","url":null,"abstract":"CD8+ T cell dysfunction is a major obstacle to hepatitis B virus (HBV) clearance and antitumor immunity. Here, using a humanized mouse model, we identify a T cell receptor targeting a clinically relevant HBV epitope and reveal ANKRD11 as a key epigenetic regulator of CD8+ T cell dysfunction in chronic infection and tumors. Ankrd11 knockout in CD8+ T cells enhances HBV-specific T cell proliferation and effector differentiation, especially under immunosuppressive conditions, via AP-1 family gene upregulation. Loss of Ankrd11 both drives the conversion of progenitor exhausted T cells into terminally exhausted T cells, and reprograms PD-1−TOX− tolerant cells into functional effectors, improving antiviral and antitumor responses. Ankrd11-deficient T cells show increased granzyme and superior effector function, enhancing viral control and tumor regression. These findings position ANKRD11 as a promising immunotherapy target for chronic HBV infection and cancer. CD8+ T cell dysfunction is a major obstacle to hepatitis B virus (HBV) clearance and antitumor immunity. Zhou and colleagues identify a T cell receptor targeting a clinically relevant HBV epitope and reveal ANKRD11 as a key epigenetic regulator of CD8+ T cell dysfunction in chronic infection and tumors.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"2006-2016"},"PeriodicalIF":26.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148932645","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}

{"title":"Dendritic cells sense microbial adhesion to launch innate immunity.","authors":"","doi":"10.1038/s41590-026-02670-9","DOIUrl":"https://doi.org/10.1038/s41590-026-02670-9","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":" ","pages":""},"PeriodicalIF":26.5,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930651","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}