Nature Immunology最新文献

{"title":"Author Correction: IL-17D-induced inhibition of DDX5 expression in keratinocytes amplifies IL-36R-mediated skin inflammation","authors":"Xinhui Ni, Yi Xu, Wang Wang, Baida Kong, Jian Ouyang, Jiwei Chen, Man Yan, Yawei Wu, Qi Chen, Xinxin Wang, Hongquan Li, Xiaoguang Gao, Hongquan Guo, Lian Cui, Zeyu Chen, Yuling Shi, Ronghui Zhu, Wei Li, Tieliu Shi, Lin-Fa Wang, Jinling Huang, Chen Dong, Yuping Lai","doi":"10.1038/s41590-026-02636-x","DOIUrl":"10.1038/s41590-026-02636-x","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 10","pages":"2172-2172"},"PeriodicalIF":26.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02636-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795760","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":"Where risk resides","authors":"Evangelos Andreakos, Ioanna Tzoulaki","doi":"10.1038/s41590-026-02621-4","DOIUrl":"10.1038/s41590-026-02621-4","url":null,"abstract":"A comprehensive atlas of tissue-resident immune cells reveals where disease-risk variants regulate gene expression, helping connect genome-wide association study signals to disease mechanisms.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1782-1784"},"PeriodicalIF":26.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795742","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":"A NOD2 to the endothelium for protective gut immunity","authors":"Susan Westfall, Irah L. King","doi":"10.1038/s41590-026-02626-z","DOIUrl":"10.1038/s41590-026-02626-z","url":null,"abstract":"Endothelial cells form the cell migration highways between organs. New results demonstrate that NOD2-dependent microbial sensing by these structural cells promotes antigen-specific T cell accumulation in gut-associated lymphoid tissues and protective mucosal immunity.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1778-1779"},"PeriodicalIF":26.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795818","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":"Mind the Notch as AXL+ DC3s creep through the gap","authors":"Purbita Bandopadhyay, Sourav Ghosh, Carla V. Rothlin","doi":"10.1038/s41590-026-02625-0","DOIUrl":"10.1038/s41590-026-02625-0","url":null,"abstract":"Notch2 deletion in dendritic cells (DCs), already known to impair type 2a DC development and intestinal immunity, is now demonstrated to promote dysbiosis and unleash inflammatory AXL-expressing type 3 DCs, driving preclinical autoimmunity.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1776-1777"},"PeriodicalIF":26.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795810","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":"Potent type-specific de novo antibodies complement broadly reactive imprinted antibodies in immune responses to SARS-CoV-2 variants","authors":"Timothy S. Johnston, Shuk Hang Li, Mark M. Painter, Divya Swaminathan, Reilly K. Atkinson, Bernadeta Dadonaite, Shuishu Wang, Naomi R. Douek, Lucas Kampman, Robin Schlesinger, Rachel Kazmierski, Bob C. Lin, Leonid A. Serebryannyy, Haijuan Du, Amy R. Henry, Sarah C. Smith, Farida Laboune, I-Ting Teng, Lingshu Wang, Nicole A. Doria-Rose, Chaim A. Schramm, Theodore C. Pierson, Tongqing Zhou, Jesse D. Bloom, E. John Wherry, Scott E. Hensley, Daniel C. Douek","doi":"10.1038/s41590-026-02613-4","DOIUrl":"10.1038/s41590-026-02613-4","url":null,"abstract":"For rapidly mutating viruses such as influenza viruses and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), immune memory recalled by antigenically drifted variants primarily comprises antibodies that cross-react to the priming strain rather than de novo elicited responses, a phenomenon termed original antigenic sin or immune imprinting. The composition and functionality of de novo responses elicited by variant exposures remain unclear. Here we isolated and characterized hundreds of recall and de novo neutralizing monoclonal antibodies after sequential exposures to SARS-CoV-2 variants in ancestral-imprinted humans. De novo variant type-specific antibodies used different V(D)J genes that were closer to germline sequence, potently neutralized future variants and targeted distinct receptor binding domain epitopes compared to ancestral cross-reactive (recall) antibodies. Nevertheless, neutralizing responses to the updated 2024–2025 booster were predominantly ancestral cross-reactive. These results reveal the distinct contributions of recall and de novo antibodies to a balanced immune response and underscore the benefit of updated booster vaccines, which augment both subsets. Updated SARS-CoV-2 boosters broaden humoral immunity by recalling cross-reactive antibodies and eliciting new less cross-reactive Omicron type-specific antibodies that target distinct RBD epitopes and more potently neutralize recent variants.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1874-1886"},"PeriodicalIF":26.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02613-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148728989","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":"Immune imprinting in a changing world","authors":"Daniel M. Altmann, Rosemary J. Boyton","doi":"10.1038/s41590-026-02629-w","DOIUrl":"10.1038/s41590-026-02629-w","url":null,"abstract":"Research on SARS-CoV-2 shows that effective immunity can arise from a balance between recalling existing immune memory and generating new variant-specific antibodies, with important implications for designing future vaccines.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1773-1775"},"PeriodicalIF":26.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148762337","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":"Accelerating the research response to the Bundibugyo virus emergency","authors":"Mariah P. Csolle, Bronwyn A. Bailey, Yuna Chung, Tsharni R. Zazryn, Tari Turner, David S. Khoury, Miles P. Davenport","doi":"10.1038/s41590-026-02623-2","DOIUrl":"10.1038/s41590-026-02623-2","url":null,"abstract":"In the context of a Public Health Emergency of International Concern, such as the Bundibugyo virus outbreak, the research community requires rapid access to information to guide an effective response. Evidence mapping brings together the available knowledge in a field into a single, organized resource, enabling researchers to rapidly identify priorities, gaps and opportunities for action.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1765-1766"},"PeriodicalIF":26.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02623-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148765012","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":"Peyer’s patch M cells organize an epithelial niche that sustains group 3 innate lymphoid cells and IL-22","authors":"Wang H. J. Cao, Yue You, Nancy Wang, M. Zeeshan Chaudhry, Huiyang Yu, Peter T. Bell, Ellesandra C. Noye, Renae Denman, Byungchul Lee, Abbey Waddington, Junpeng Ye, Jaring Schreuder, Qiutong Huang, Julie Tellier, Sophie Curio, James Santiago, Daniela Amann-Zalcenstein, Nicolas Jacquelot, Peter Hickey, Stephen L. Nutt, Cyril Seillet, Philip M. Hansbro, Verena C. Wimmer, Richard A. Strugnell, Zewen Kelvin Tuong, Matthew E. Richie, Gabrielle T. Belz","doi":"10.1038/s41590-026-02606-3","DOIUrl":"10.1038/s41590-026-02606-3","url":null,"abstract":"Microfold (M) cells transcytose luminal antigens to initiate mucosal adaptive immunity, but their role in organizing innate responses in Peyer’s patches is unclear. Here we showed that Peyer’s patch M cells organized an epithelial–group 3 innate lymphoid cell (ILC3) axis, establishing a spatial niche within the dome epithelium that drove ILC3 localization, proliferation and IL-22 production. We found that epithelial, but not hematopoietic, SPI-B was required for intestinal IgA responses to establish this niche. Single-cell profiling of intestinal SPI-B+ epithelial cells revealed that M cells were highly heterogeneous, displaying tissue- and pathogen-specific transcriptional programs. Using subset-specific genetic perturbation and whole-mount imaging, we found that this circuit relied on CCR6-dependent positioning cues and RANK–RANKL signaling to ILC3 to regulate Peyer’s patch ILC3 homeostasis. Together, these findings identified Peyer’s patch M cells as organizers that spatially coordinated innate cell localization, proliferation and cytokine production to maintain mucosal barrier defense. Belz and colleagues show that Peyer’s patch M cells are required for ILC3 localization, proliferation and IL-22 production within the dome epithelium.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1829-1841"},"PeriodicalIF":26.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02606-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148728988","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":"TIF1γ holds the line against regulatory T cell plasticity","authors":"Fotini Gounari, Khashayarsha Khazaie","doi":"10.1038/s41590-026-02620-5","DOIUrl":"10.1038/s41590-026-02620-5","url":null,"abstract":"A mechanistic understanding of how regulatory T cell plasticity is controlled remains lacking. A study shows that TIF1γ modulates this plasticity by restraining β-catenin signaling.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1780-1781"},"PeriodicalIF":26.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148766369","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":"Epigenetic modulation of stromal cell states underpins pathological tissue niches in Crohn’s disease","authors":"Simon Koplev, Osheen Sharma, Simon Woelfel, Ni Huang, Mathilde Pohin, Adrian Feile, Maria Warschinke, Mikel Rezola Artero, Sharujan Suthakaran, Ioannis Sarropoulos, J. Patrick Pett, Julia Nyman, Tom Thomas, Duy Pham, Bin Li, Moustafa Attar, Julia Pakpoor, Kate Milosevic-Hutton, Alistair Easton, Matt Butler, James Dunford, Martin Philpott, Mark Coles, Christopher D. Buckley, Calliope Dendrou, Khalid Shamiyah, Lorenz Kretschmer, Lisa Dratva, Fadi Issa, Joanna Hester, Jens Rittscher, Alissa Walsh, Simon P. Travis, Fränze Progatzky, Lukas W. Unger, Mark Bignell, Katherine Baker, Bruce George, Hussein Al-Mossawi, Paul Klenerman, Alexander S. Mosig, Udo Oppermann, Sarah A. Teichmann, Fiona M. Powrie, Matthias Friedrich","doi":"10.1038/s41590-026-02617-0","DOIUrl":"10.1038/s41590-026-02617-0","url":null,"abstract":"Stromal cell states are altered in active Crohn’s disease (CD), but their origin and phenotypic stability are unknown. Using single-cell spatial transcriptomics, RNA sequencing and ATAC sequencing of ~2,500,000 cells, we map 18 distinct stromal cell states within their cellular and cytokine signaling environments in human full-thickness CD bowel. Inflammatory fibroblasts (IFs) reside in immune cell-rich mucosal ulcers and are induced through combinatorial cytokine exposure suppressing submucosal universal fibroblast programs. The IF state is stabilized through transcription factor (TF) activity of GLI3, TWIST1, ETV4, PRDM1 and RELB, and does not spontaneously revert; however, histone deacetylase inhibition destabilizes the IF state, preventing IF secretome-induced epithelial transmigration and activation of neutrophils. The IF open chromatin configuration is distinct from that of fibrotic contractile stroma, which populate adjoining immune-depleted submucosal fibrotic niches. These findings show that microenvironments in pathological tissue niches shape open chromatin configuration of stromal states that are amenable to modulation by epigenetic modifiers. The authors provide a multiomic single-cell and spatial atlas of Crohn’s disease, focusing on the crosstalk between immune and stromal cells and heterogeneity around mucosal lesions.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"27 9","pages":"1954-1968"},"PeriodicalIF":26.5,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41590-026-02617-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148723248","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}