{"title":"Citraconate preserves T cell stemness and antitumor immunity","authors":"Wenhui Li, Minmin Ge, Ziyi Luo, Minju Ni, Kexin Tang, Chenfeng Han, Jiajia Wang, Yifu Ma, Xiaowei Liu, Kaili Ma, Jingxing Yang, Wenjing Li, Cangang Zhang, Qitai Zhao, Guangcan Shao, Jaeoh Park, Yi Zhang, Yonghong Wan, Baojun Zhang, Gang Wang, Mingjing Shen, Qiang Shan, Feng Guo, Ping-Chih Ho, Liyuan Zhang, Lianjun Zhang","doi":"10.1126/sciimmunol.adz0348","DOIUrl":"10.1126/sciimmunol.adz0348","url":null,"abstract":"<div >Metabolic perturbations in the tumor microenvironment profoundly compromise the stemlike properties and effector functions of CD8 T cells. Deciphering the metabolic circuitry that sustains T cell stemness is critical for reinvigorating tumor-infiltrating lymphocytes and augmenting immunotherapeutic efficacy. Here, we identify citraconate, an itaconate isomer, as a metabolite markedly depleted in CD8 T cells subjected to chronic antigen stimulation or hypoxic conditions. Citraconate supplementation preserves stemlike characteristics, attenuates ferroptosis, and potentiates T cell–mediated antitumor immunity. Mechanistically, citraconate maintains intracellular cyclic adenosine monophosphate (cAMP) concentrations by suppressing phosphodiesterase1A/C (PDE1A/C) expression and preserving mitochondrial integrity, thereby activating protein kinase A (PKA) signaling. This activation transcriptionally represses arachidonate-5-lipoxygenase (ALOX5), consequently reducing arachidonic acid peroxidation. Clinically, diminished ALOX5 or PDE1A expression correlates with reduced T cell exhaustion and improved responses to immune checkpoint blockade (ICB) therapy. Our findings reveal the citraconate-mediated PDE1-cAMP-ALOX5 axis as a potential therapeutic target for enhancing cancer immunotherapy.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 119","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147820529","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}
Ronan Kapetanovic, Syeda Farhana Afroz, James E. B. Curson, Ina Kirmes, Divya Ramnath, Stephan Nothjunge, Jinting Liu, Jordan D. Atkinson, Arnaud Ahier, Karoline D. Raven, Marta Bosch, Bernhard Keller, Grace M. E. P. Lawrence, Kaustav Das Gupta, Melanie R. Shakespear, Charles Ferguson, Claudia J. Stocks, Nilesh J. Bokil, Gabriele Matthias, Tam T. K. Nguyen, Zeinab G. Khalil, Robert C. Reid, Karl A. Hansford, Philip M. Hansbro, Matthew A. Cooper, Mark A. Schembri, Antje Blumenthal, Kate Schroder, David P. Fairlie, Albert Pol, Patrick Matthias, Robert G. Parton, Steven Zuryn, Matthew J. Sweet
{"title":"Mitochondrial fission mediates an evolutionarily conserved antibacterial defense response","authors":"Ronan Kapetanovic, Syeda Farhana Afroz, James E. B. Curson, Ina Kirmes, Divya Ramnath, Stephan Nothjunge, Jinting Liu, Jordan D. Atkinson, Arnaud Ahier, Karoline D. Raven, Marta Bosch, Bernhard Keller, Grace M. E. P. Lawrence, Kaustav Das Gupta, Melanie R. Shakespear, Charles Ferguson, Claudia J. Stocks, Nilesh J. Bokil, Gabriele Matthias, Tam T. K. Nguyen, Zeinab G. Khalil, Robert C. Reid, Karl A. Hansford, Philip M. Hansbro, Matthew A. Cooper, Mark A. Schembri, Antje Blumenthal, Kate Schroder, David P. Fairlie, Albert Pol, Patrick Matthias, Robert G. Parton, Steven Zuryn, Matthew J. Sweet","doi":"10.1126/sciimmunol.aed2623","DOIUrl":"10.1126/sciimmunol.aed2623","url":null,"abstract":"<div >Animals engage pleiotropic immune defense mechanisms to survive infections. Here, we present a function for mitochondrial fission in host defense. Challenge of macrophages with <i>Escherichia coli</i> increased mitochondrial fission, with this response promoting bacterial clearance in mammalian macrophages and <i>Caenorhabditis elegans</i>. <i>E. coli</i>–induced mitochondrial fission engaged dual antibacterial responses via the mitochondrial unfolded protein response (UPR<sup>mt</sup>) and inducible lipid droplet production. Mitochondrial fission–triggered UPR<sup>mt</sup>, characterized by activation of activating transcription factor 5 (ATF5) in mouse macrophages and the paralog ATFS-1 in <i>C. elegans</i>, curtailed inducible lipid droplets to cross-regulate these pathways. The intramacrophage pathogen <i>Salmonella enterica</i> suppressed antibacterial mitochondrial fission, but restoring this response by inhibiting mitochondrial fusion–promoting histone deacetylase 6 (HDAC6) reactivated lipid droplet production and bacterial clearance. Therefore, we propose that mitochondrial fission is an ancient host defense pathway that can be exploited for anti-infective design.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147736620","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":"Erratum for the Research Article “The chemerin-CMKLR1 axis limits thermogenesis by controlling a beige adipocyte/IL-33/type 2 innate immunity circuit”","authors":"","doi":"10.1126/sciimmunol.aeh5833","DOIUrl":"10.1126/sciimmunol.aeh5833","url":null,"abstract":"","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147738959","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}
Allen W. Ho, Linglin Huang, Sumiti Sandhu, Sheng Xiao, Melissa Sgodzai, Ella Ullerich, Rajesh K. Krishnan, Alexandra Schnell, Vijay K. Kuchroo
{"title":"An adaptive cellular source of IL-17A and IL-17F is critical for the induction of experimental autoimmune encephalomyelitis","authors":"Allen W. Ho, Linglin Huang, Sumiti Sandhu, Sheng Xiao, Melissa Sgodzai, Ella Ullerich, Rajesh K. Krishnan, Alexandra Schnell, Vijay K. Kuchroo","doi":"10.1126/sciimmunol.aee1481","DOIUrl":"10.1126/sciimmunol.aee1481","url":null,"abstract":"<div >T helper 17 (T<sub>H</sub>17) cells are thought to play an important role in the pathogenesis of many autoimmune disorders, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). However, recent studies have suggested that interleukin-17 (IL-17) may be dispensable for the induction of EAE. Here, we use an adoptive transfer model of EAE to demonstrate that an adaptive cellular source of IL-17 is absolutely required for the induction of EAE disease. We further show that B cells can regulate the transfer of EAE disease in this context. Transcriptional profiling of T<sub>H</sub>17 cells in our model suggests that loss of IL-17A/F in T cells results in a lack of an IL-23 receptor (IL-23R)–driven signaling signature. Our data demonstrate the critical importance of an adaptive immune cellular source of IL-17A and IL-17F to mediate EAE and that IL-17 signaling is required for IL-23–mediated T<sub>H</sub>17 cell pathogenicity.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147736782","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}
Esther L. Jones Evans, Benjamin Demarco, Han Cai, Madelon M.E. de Jong, Sarah Hill, Marcus A. Widdess, Joannah R. Fergusson, Ryan E. Glass, Gemma Harris, Gracie J. Mead, Yavuz F. Yazicioglu, Saba Nayar, Benjamin A. Fisher, Mark S. Cragg, Alexander J. Clarke, Audrey Gérard, Jelena S. Bezbradica, Lynn B. Dustin
{"title":"The autoantigen TRIM21 assembles proinflammatory immune complexes after lytic cell death","authors":"Esther L. Jones Evans, Benjamin Demarco, Han Cai, Madelon M.E. de Jong, Sarah Hill, Marcus A. Widdess, Joannah R. Fergusson, Ryan E. Glass, Gemma Harris, Gracie J. Mead, Yavuz F. Yazicioglu, Saba Nayar, Benjamin A. Fisher, Mark S. Cragg, Alexander J. Clarke, Audrey Gérard, Jelena S. Bezbradica, Lynn B. Dustin","doi":"10.1126/sciimmunol.ads9680","DOIUrl":"10.1126/sciimmunol.ads9680","url":null,"abstract":"<div >Sjögren’s disease (SjD) causes localized and systemic inflammation and autoantibody production against intracellular proteins such as TRIM21/Ro52 (tripartite motif-containing protein 21). TRIM21, an E3 ubiquitin ligase, binds antibody Fc domains on opsonized pathogens that have escaped extracellular immunity and entered the cytosol. TRIM21 then ubiquitinates these pathogens, driving their proteasomal degradation. How TRIM21 becomes an autoantigen remains unclear. We show that TRIM21 is released upon lytic cell death (pyroptosis or necroptosis) but not apoptosis. Although many cytosolic proteins are released by dead cells, liberated TRIM21 is distinct: Its high antibody affinity enables binding to Fc domains of circulating immunoglobulins, forming large immune complexes (ICs). These ICs increase in SjD, where anti-TRIM21 autoantibodies interact with released TRIM21 via Fc and F(ab′)<sub>2</sub>. TRIM21 ICs are taken up by macrophages, which drive proinflammatory responses, antigen presentation, and metabolic changes in high interferon environments. Thus, TRIM21 may perpetuate inflammation and autoantigen presentation, resulting in high immunogenicity.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695559","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}
Ntombizodwa Makuyana, Laura Seldeslachts, Lauren Michiels, Oliver T. Burton, Alvaro R. Hernandez, Arman Ghodsinia, Ekhlas Rahman, Laura M. Kops, Kailash Singh, Fran Naranjo, Magda Ali, Amy Dashwood, Marwane Achkir, Lubna Kouser, Stephanie Lienart, Stephane Guillaume, Lieve Naesens, Michelle A. Linterman, Joost Wauters, Régis Joulia, Stephanie Humblet-Baron, Greetje Vande Velde, James Dooley, Adrian Liston
{"title":"Gene delivery of immunomodulatory cytokines to the lung preserves respiratory function during inflammatory challenge","authors":"Ntombizodwa Makuyana, Laura Seldeslachts, Lauren Michiels, Oliver T. Burton, Alvaro R. Hernandez, Arman Ghodsinia, Ekhlas Rahman, Laura M. Kops, Kailash Singh, Fran Naranjo, Magda Ali, Amy Dashwood, Marwane Achkir, Lubna Kouser, Stephanie Lienart, Stephane Guillaume, Lieve Naesens, Michelle A. Linterman, Joost Wauters, Régis Joulia, Stephanie Humblet-Baron, Greetje Vande Velde, James Dooley, Adrian Liston","doi":"10.1126/sciimmunol.adv7969","DOIUrl":"10.1126/sciimmunol.adv7969","url":null,"abstract":"<div >Respiratory infections that result in severe and life-threatening immune-mediated respiratory decline are a major public health issue. Controlling local respiratory immune reactions without the use of systemic immunosuppressants remains an unmet clinical challenge. We developed a gene delivery system to express anti-inflammatory cytokines in the lung, which reestablishes local immune homeostasis without triggering systemic effects. Using an adeno-associated vector cargo system (AAV6.2-<i>CC10</i>), we induced production of interleukin-2 (IL-2), IL-1 receptor antagonist (IL-1RA), and IL-10 in situ in the lung microenvironment, with no detectable expression or immunological deviation in the peripheral immune system. We demonstrate the effective potential of IL-2, IL-1RA, and IL-10 as immunomodulatory cargos in severe infectious challenge, which reduced respiratory pathology after influenza-associated pulmonary aspergillosis. Thus, the AAV6.2-<i>CC10</i> platform enables targeted delivery of biologics to the lung, modulates the lung environment, and improves pathology without inducing systemic immune reactions.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695557","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}
Carlos Silvestre-Roig, Raphael Chevre, Merieme Farjia, Alexander Bender, Lina M. Vöcking, Mathis Richter, Ali Hageb, Vincent Suerdieck, Francisco J. Arenas Cerro, Quinte Braster, Mauricio Guzman, Jordi Sintes, Samriti Sharma, Patricia Lemnitzer, Claudia Tulotta, Yvonne Börgeling, Andrea Herrero-Cervera, Hannah Flueter, Sara Noemi Reinartz Groba, David Ahern, Collins Osei-Sarpong, Ralf Zimmer, Noelia Alonso-Gonzalez, Eduardo Ortega, Stefan Lienenklaus, Ulrich Kalinke, Stephan Ludwig, Daniel R. Engel, Frank Rosenbauer, Claudia Monaco, Petra Dersch, Artur Kibler, Andrea Cerutti, Triantafyllos Chavakis, Rui Benedito, Andres Hidalgo, Jadwiga Jablonska, Miguel Palomino-Segura, Oliver Soehnlein
{"title":"Divergent granulopoiesis at extramedullary sites safeguards antibacterial host defense","authors":"Carlos Silvestre-Roig, Raphael Chevre, Merieme Farjia, Alexander Bender, Lina M. Vöcking, Mathis Richter, Ali Hageb, Vincent Suerdieck, Francisco J. Arenas Cerro, Quinte Braster, Mauricio Guzman, Jordi Sintes, Samriti Sharma, Patricia Lemnitzer, Claudia Tulotta, Yvonne Börgeling, Andrea Herrero-Cervera, Hannah Flueter, Sara Noemi Reinartz Groba, David Ahern, Collins Osei-Sarpong, Ralf Zimmer, Noelia Alonso-Gonzalez, Eduardo Ortega, Stefan Lienenklaus, Ulrich Kalinke, Stephan Ludwig, Daniel R. Engel, Frank Rosenbauer, Claudia Monaco, Petra Dersch, Artur Kibler, Andrea Cerutti, Triantafyllos Chavakis, Rui Benedito, Andres Hidalgo, Jadwiga Jablonska, Miguel Palomino-Segura, Oliver Soehnlein","doi":"10.1126/sciimmunol.adw7077","DOIUrl":"10.1126/sciimmunol.adw7077","url":null,"abstract":"<div >Extramedullary organs such as the spleen can assume granulopoiesis as a supportive mechanism to cope with increased demands during persistent inflammation. However, the quantitative output of extramedullary granulopoiesis is limited, and whether the spleen provides neutrophils of a qualitative difference remains unclear. Here, we found that splenic stress granulopoiesis is associated with distinct neutrophil production and differentiation trajectories. Myeloid progenitors in the spleen engaged in accelerated production of neutrophils with an immature phenotype. Yet, neutrophils generated during persistent stress granulopoiesis were fully competent to exert antimicrobial functions and were necessary to contain bacterial invasion in the bladder. Activation of type I interferon signaling in the spleen was required for splenic neutrophil priming, and its loss impaired antibacterial host defense. Thus, the spleen provides an immunological environment for stress-induced rapid production and priming of highly active neutrophils to meet demands during infection.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695675","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}
Kelli A. McCord, Emerald Kan, Sean Hyslop, Amanda Y. Xia, Colby J. Hofferek, James S. Lewis Jr., Andreas Wieland, David J. Hernandez, Vlad C. Sandulache, William H. Hudson
{"title":"Single-cell TCR mapping reveals spatially coordinated T cell states in head and neck cancer","authors":"Kelli A. McCord, Emerald Kan, Sean Hyslop, Amanda Y. Xia, Colby J. Hofferek, James S. Lewis Jr., Andreas Wieland, David J. Hernandez, Vlad C. Sandulache, William H. Hudson","doi":"10.1126/sciimmunol.aec3133","DOIUrl":"10.1126/sciimmunol.aec3133","url":null,"abstract":"<div >Current spatial T cell receptor (TCR) profiling approaches lack the resolution needed to link clonal identity, transcriptional state, and spatial positioning of individual T cells in the tumor microenvironment. Here, we introduce a spatial TCR profiling strategy that resolves individual T cell clones together with their transcriptional states at single-cell resolution and applied the method to human head and neck squamous cell carcinoma. Presumed tumor-specific T cells were broadly dispersed throughout the tumor microenvironment, and cells of the same clone occupied distinct transcriptional states in different locations: Immune-rich regions contained more plastic or progenitor cells, whereas tumor-dense regions were enriched for exhausted states. Patients exhibited notably different spatial architectures of antitumor T cell responses, revealing variation that was not captured by high-resolution, spatially agnostic methods such as spectral flow cytometry and single-cell RNA sequencing. These results provide a blueprint for dissecting antigen-specific T cell states in human tumors and reveal how T cell states are spatially coordinated with local cues across the tumor microenvironment.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643270","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}
Chenyu Zhang, Charles Chien, Eglė Jurgaitytė, Koharu Sakiyama, Alissa Bockman, Yeara Jo, Seungwon Lee, Stephanie Silveria, Elizabeth Andrews, Abigail Mende, Lily Zhang, K. Christopher Garcia, Allon Wagner, Michel DuPage, David Raulet
{"title":"Intratumoral Treg cell ablation elicits NK cell–mediated control of CD8 T cell–resistant tumors","authors":"Chenyu Zhang, Charles Chien, Eglė Jurgaitytė, Koharu Sakiyama, Alissa Bockman, Yeara Jo, Seungwon Lee, Stephanie Silveria, Elizabeth Andrews, Abigail Mende, Lily Zhang, K. Christopher Garcia, Allon Wagner, Michel DuPage, David Raulet","doi":"10.1126/sciimmunol.adx4411","DOIUrl":"10.1126/sciimmunol.adx4411","url":null,"abstract":"<div >Cancer cells frequently lose major histocompatibility complex class I (MHC I) to evade CD8 T cell recognition. Natural killer (NK) cells are poised to target MHC I–deficient cancer cells, but MHC I loss alone is often insufficient to unleash fully effective NK cell responses. Here, we show that selective intratumoral (IT) ablation of regulatory T cells (T<sub>reg</sub> cells) elicited potent antitumor NK cell responses that controlled MHC I–deficient and even MHC I<sup>+</sup> cancers that expressed NKG2D ligands. T<sub>reg</sub> cells controlled the activation, maturation, and antitumor cytotoxic activity of NK cells within the tumor microenvironment. Mechanistically, depletion of IT-T<sub>reg</sub> cells relieved the inhibition of cDC2-dependent induction of IL-2 production by conventional CD4 T cells that was necessary for NK cell activation. Systemically administered antibodies that selectively depleted IT-T<sub>reg</sub> cells similarly empowered NK cell–dependent tumor control. These findings expand the breadth of T<sub>reg</sub> cell–mediated cancer immunosuppression to encompass antitumor NK cells and suggest that therapeutic targeting of T<sub>reg</sub> cells in tumors can control CD8 T cell–resistant cancers.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643269","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":"Erratum for the Research Article “A noncanonical cytoplasmic role for BUB1 in restraining DNA damage–induced dsRNA accumulation and sensing within stress granules”","authors":"","doi":"10.1126/sciimmunol.aeh4448","DOIUrl":"10.1126/sciimmunol.aeh4448","url":null,"abstract":"","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"11 118","pages":""},"PeriodicalIF":16.3,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147643267","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}
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