Nature Immunology最新文献

{"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}

{"title":"Author Correction: A novel CAF population coordinates hyper-suppressive regulatory T cell recruitment and localization in lung cancer.","authors":"Olivia R Ringham, Monica Rivera, Lucas F Loffredo, Melih Arda Ozsoy, Christina M Healy, Maye F Cheng, Yinuo Jin, Noah Chen, Kenia de Los Santos-Alexis, Elham Azizi, Anjali Saqi, Matthew B Buechler, Carla P Concepcion-Crisol, Nicholas Arpaia","doi":"10.1038/s41590-026-02680-7","DOIUrl":"https://doi.org/10.1038/s41590-026-02680-7","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":"148930645","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":"The overlooked plasticity of monocytes in uterine homeostasis","authors":"","doi":"10.1038/s41590-026-02658-5","DOIUrl":"10.1038/s41590-026-02658-5","url":null,"abstract":"Myeloid cell immunophenotyping in women and functional studies in mice indicated that monocytes contribute to both inflammation and tissue remodeling in the uterus and dynamically regulate tissue homeostasis throughout the reproductive cycle. Dysregulation of monocyte function was associated with uterine fibrosis (Asherman’s syndrome), which has severe consequences for reproductive health.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"1994-1995"},"PeriodicalIF":26.5,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920711","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":"AMBRA1 allosterically activates NLRP3 by releasing its autoinhibition","authors":"Minghui Pan, Jie Zhou, Shuo Fu, Yuluan Tang, Gonglu Zou, Pilong Li, Zhengfan Jiang","doi":"10.1038/s41590-026-02644-x","DOIUrl":"10.1038/s41590-026-02644-x","url":null,"abstract":"Nod-like receptor family pyrin domain-containing 3 (NLRP3) is activated by many stimuli, and its dysfunction is involved in various inflammatory diseases. Activation of NLRP3 is thought to happen via a multistep process involving phase separation, conformational opening and oligomerization. However, how NLRP3 is released from its autorepressed conformation remains elusive. Here we report that activating molecule in Beclin1-regulated autophagy protein 1 (AMBRA1), previously known for its role in autophagy, bound NLRP3 to scaffold and allosterically activate NLRP3. AMBRA1 engaged the leucine-rich repeat and helical domain 2 subdomains of NLRP3 through its β-propeller domain and destabilized the closed, inactive conformation of NLRP3, facilitating adenosine triphosphate binding and transition of NLRP3 to the active state. AMBRA1 deficiency in monocytes or macrophages impaired NLRP3 activation and reduced inflammatory responses in mouse models of endotoxic shock, colitis and sepsis. Nanobodies blocking the interaction between AMBRA1 and NLRP3 inhibited NLRP3 activation, underscoring the therapeutic potential of targeting this interaction. Our study revealed the role of AMBRA1 in NLRP3 inflammasome assembly and activation, offering potential pharmacological targets for related diseases. Jiang and colleagues show that the adaptor protein AMBRA1 binds NLRP3 to destabilize the closed, inactive conformation of NLRP3 and facilitate binding of ATP and transition to the active state of NLRP3.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"2017-2028"},"PeriodicalIF":26.5,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920670","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}