Nature Immunology最新文献

{"title":"Mapping STING","authors":"Nicholas J. Bernard","doi":"10.1038/s41590-025-02128-4","DOIUrl":"10.1038/s41590-025-02128-4","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"528-528"},"PeriodicalIF":27.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741702","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":"Peroxisomes mediate tissue repair","authors":"Stephanie Houston","doi":"10.1038/s41590-025-02130-w","DOIUrl":"10.1038/s41590-025-02130-w","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"528-528"},"PeriodicalIF":27.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741706","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":"Building immune barriers","authors":"Laurie A. Dempsey","doi":"10.1038/s41590-025-02127-5","DOIUrl":"10.1038/s41590-025-02127-5","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"528-528"},"PeriodicalIF":27.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741705","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":"IFNλ drives diarrhea","authors":"Paula Jauregui","doi":"10.1038/s41590-025-02129-3","DOIUrl":"10.1038/s41590-025-02129-3","url":null,"abstract":"","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"528-528"},"PeriodicalIF":27.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741704","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":"Overcoming TGFβ and activin A suppression boosts NK cell antitumor function","authors":"","doi":"10.1038/s41590-025-02112-y","DOIUrl":"10.1038/s41590-025-02112-y","url":null,"abstract":"Natural killer (NK) cell function is suppressed by transforming growth factor-β (TGFβ) and activin A. Knockout of the common signaling mediator SMAD4 by CRISPR–Cas9 resulted in NK cells with enhanced antitumor activity, offering a strategy for improving NK cell-based cancer immunotherapies.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"540-541"},"PeriodicalIF":27.7,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712982","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":"An SSTR2–somatostatin chemotactic axis drives T cell progenitor homing to the intestines","authors":"Borja Ocón, Kevin F. Brulois, Husein Hadeiba, Mohammed Gaafarelkhalifa, Aiman Ayesha, Yuhan Bi, Menglan Xiang, Jacob Gulman, Maryam Kooshesh, Junliang Pan, Eugene C. Butcher","doi":"10.1038/s41590-025-02097-8","DOIUrl":"10.1038/s41590-025-02097-8","url":null,"abstract":"Progenitors of intraepithelial T cells (IELps) migrate from the thymus to the intestines after birth where they develop into unconventional TCRγδ and TCRαβ lymphocytes in a process of extrathymic lymphopoiesis within cryptopatches. Mechanisms of IELp migration have remained unclear. Here we show that thymic IELps express the somatostatin receptor SSTR2, which contributes to their homing to the gut. IELp homing is Sstr2 dependent and correlates with neonatal induction of Sst encoding somatostatin in neuroendocrine and lamina propria stromal cells. The SSTR2 ligands somatostatin and cortistatin attract IELps in chemotaxis assays and somatostatin triggers IELp binding to the mucosal vascular addressin MAdCAM1. T cell transduction with Sstr2 confers homing to the neonatal colon. Human fetal thymic IELp-like cells express SSTR2 and intestinal stromal cells express SST at the time of initial T cell population, suggesting conserved mechanisms of progenitor seeding of the developing intestines. These results reveal an unexpected role for the SSTR2–somatostatin axis in early immune system development and describe a new role for a small peptide hormone G-protein-coupled receptor in developmental lymphocyte trafficking. Progenitors of intraepithelial T cells (IELps) migrate from the thymus to the intestines after birth where they can develop into unconventional intraepithelial lymphocytes. Here Ocon et al. find that the neuroendocrine peptide hormone somatostatin controls the migration of committed SSTR2-expressing IELps from the thymus to the immature gut.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"607-618"},"PeriodicalIF":27.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702908","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":"ImmGenMaps, an open-source cartography of the immune system","authors":"Miguel Reina-Campos, Samouil L. Farhi, Christophe Benoist","doi":"10.1038/s41590-025-02119-5","DOIUrl":"https://doi.org/10.1038/s41590-025-02119-5","url":null,"abstract":"<p>The Immunological Genome Project Consortium (ImmGen) is announcing the launch of ImmGenMaps (https://www.immgen.org/ImmGenMaps), a project designed to spatially profile every immune cell across the mouse anatomy. This community project builds upon the bulk and single-cell profiling efforts of ImmGen to characterize the genetic regulation of all cells of the mouse immune system. Using state-of-the-art spatial transcriptomics technology, ImmGenMaps goes one step further by profiling immune cells within their natural environments across all major organs, at baseline or under challenge. In addition to capturing transcriptional profiles and a subset of landmark protein markers of immunocytes, ImmGenMaps will also profile non-immune cells (stroma, epithelia, connective tissue), whose key roles in orchestrating immune function is increasingly recognized. By capturing the pieces of the immune game (immune cells) and the playing board (tissue structures and non-immune cells), and determining the rules that govern the immune game (environmental signals and cellular interactions), we expect to provide a key resource to the scientific community. In line with ImmGen’s previous ‘OpenSource’ projects^1,2, the intent is to leverage the broader community’s expertise by welcoming the participation of immunology and computational biology labs beyond the core ImmGen membership.</p><p>ImmGenMaps aims to broach several initial questions aimed at deepening our understanding of cellular dynamics across tissues. It seeks to profile the frequency of all immune and non-immune cell types, including those, like granulocytes, that are typically lost during tissue dissociation-based profiling. In addition, the project aims to define discrete cellular niches, spatial domains and the relevant gradients of organ function, while also unraveling the connectivity between immune cells and their surrounding cells. Further objectives include mapping the sources of key signals — such as chemokines and cytokines — in both health and disease, assessing the link between cellular location and phenotype, and conducting a rigorous evaluation of how cell types and phenotypes correlate with tissue type and location.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"14 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702915","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":"Distinct type 1 immune networks underlie the severity of restrictive lung disease after COVID-19","authors":"Glenda Canderan,&nbsp;Lyndsey M. Muehling,&nbsp;Alexandra Kadl,&nbsp;Shay Ladd,&nbsp;Catherine Bonham,&nbsp;Claire E. Cross,&nbsp;Sierra M. Lima,&nbsp;Xihui Yin,&nbsp;Jeffrey M. Sturek,&nbsp;Jeffrey M. Wilson,&nbsp;Behnam Keshavarz,&nbsp;Kyle B. Enfield,&nbsp;Chintan Ramani,&nbsp;Naomi Bryant,&nbsp;Deborah D. Murphy,&nbsp;In Su Cheon,&nbsp;Michael Solga,&nbsp;Patcharin Pramoonjago,&nbsp;Coleen A. McNamara,&nbsp;Jie Sun,&nbsp;Paul J. Utz,&nbsp;Sepideh Dolatshahi,&nbsp;Jonathan M. Irish,&nbsp;Judith A. Woodfolk","doi":"10.1038/s41590-025-02110-0","DOIUrl":"10.1038/s41590-025-02110-0","url":null,"abstract":"The variable origins of persistent breathlessness after coronavirus disease 2019 (COVID-19) have hindered efforts to decipher the immunopathology of lung sequelae. Here we analyzed hundreds of cellular and molecular features in the context of discrete pulmonary phenotypes to define the systemic immune landscape of post-COVID lung disease. Cluster analysis of lung physiology measures highlighted two phenotypes of restrictive lung disease that differed according to their impaired diffusion and severity of fibrosis. Machine learning revealed marked CCR5+CD95+CD8+ T cell perturbations in milder lung disease but attenuated T cell responses hallmarked by elevated CXCL13 in more severe disease. Distinct sets of cells, mediators and autoantibodies distinguished each restrictive phenotype and differed from those of patients without substantial lung involvement. These differences were reflected in divergent T cell-based type 1 networks according to the severity of lung disease. Our findings, which provide an immunological basis for active lung injury versus advanced disease after COVID-19, might offer new targets for treatment. This study presents a comprehensive immunological assessment of post-coronavirus disease (COVID) respiratory illness, finding signatures potentially associated with recovery and candidate biomarkers for more severe lung disease.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"595-606"},"PeriodicalIF":27.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702911","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":"Enhancing human NK cell antitumor function by knocking out SMAD4 to counteract TGFβ and activin A suppression","authors":"Anna Rea,&nbsp;Sara Santana-Hernández,&nbsp;Javier Villanueva,&nbsp;Marta Sanvicente-García,&nbsp;Mariona Cabo,&nbsp;Jesús Suarez-Olmos,&nbsp;Fabricio Quimis,&nbsp;Mengjuan Qin,&nbsp;Eduard Llorens,&nbsp;Sandra Blasco-Benito,&nbsp;Lamberto Torralba-Raga,&nbsp;Lorena Perez,&nbsp;Bishan Bhattarai,&nbsp;Elisenda Alari-Pahissa,&nbsp;Anna-Maria Georgoudaki,&nbsp;Francesc Balaguer,&nbsp;Manel Juan,&nbsp;Julián Pardo,&nbsp;Toni Celià-Terrassa,&nbsp;Ana Rovira,&nbsp;Nina Möker,&nbsp;Congcong Zhang,&nbsp;Marco Colonna,&nbsp;Jan Spanholtz,&nbsp;Karl-Johan Malmberg,&nbsp;Clara Montagut,&nbsp;Joan Albanell,&nbsp;Marc Güell,&nbsp;Miguel López-Botet,&nbsp;Aura Muntasell","doi":"10.1038/s41590-025-02103-z","DOIUrl":"10.1038/s41590-025-02103-z","url":null,"abstract":"Transforming growth factor beta (TGFβ) and activin A suppress natural killer (NK) cell function and proliferation, limiting the efficacy of adoptive NK cell therapies. Inspired by the partial resistance to TGFβ of NK cells with SMAD4 haploinsufficiency, we used CRISPR–Cas9 for knockout of SMAD4 in human NK cells. Here we show that SMAD4KO NK cells were resistant to TGFβ and activin A inhibition, retaining their cytotoxicity, cytokine secretion and interleukin-2/interleukin-15-driven proliferation. They showed enhanced tumor penetration and tumor growth control, both as monotherapy and in combination with tumor-targeted therapeutic antibodies. Notably, SMAD4KO NK cells outperformed control NK cells treated with a TGFβ inhibitor, underscoring the benefit of maintaining SMAD4-independent TGFβ signaling. SMAD4KO conferred TGFβ resistance across diverse NK cell platforms, including CD19-CAR NK cells, stem cell-derived NK cells and ADAPT-NK cells. These findings position SMAD4 knockout as a versatile and compelling strategy to enhance NK cell antitumor activity, providing a new avenue for improving NK cell-based cancer immunotherapies. The authors show that knocking out SMAD4, human NK cells resist TGFβ and activin A suppression and demonstrate that SMAD4 knockout enhances the antitumor function of several NK cell products in clinical development.","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"26 4","pages":"582-594"},"PeriodicalIF":27.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41590-025-02103-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143666293","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":"Author Correction: Transcriptional function of E2A, Ebf1, Pax5, Ikaros and Aiolos analyzed by in vivo acute protein degradation in early B cell development","authors":"Anna S. Fedl, Hiromi Tagoh, Sarah Gruenbacher, Qiong Sun, Robyn L. Schenk, Kimon Froussios, Markus Jaritz, Meinrad Busslinger, Tanja A. Schwickert","doi":"10.1038/s41590-025-02139-1","DOIUrl":"https://doi.org/10.1038/s41590-025-02139-1","url":null,"abstract":"<p>Correction to: <i>Nature Immunology</i> https://doi.org/10.1038/s41590-024-01933-7, published online 23 August 2024.</p>","PeriodicalId":19032,"journal":{"name":"Nature Immunology","volume":"183 1","pages":""},"PeriodicalIF":30.5,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143666217","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}