IF 45.1 1区生物学

Cell Pub Date : 2026-09-25 DOI: 10.1016/j.cell.2026.08.054

Joseph M Dobbs, Rasmus K Jensen, Julia Mahamid

{"title":"Single-cell visual proteomics of a minimal bacterium reveals structural coordination of gene expression machineries.","authors":"Joseph M Dobbs, Rasmus K Jensen, Julia Mahamid","doi":"10.1016/j.cell.2026.08.054","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.054","url":null,"abstract":"Translation is a central process in gene expression. Its regulation is complex, depends on factors that include cell state and the subcellular environment, and is subject to modulation via crosstalk to processes such as transcription or translocation. Here, we used cryo-electron tomography of native and antibiotic-perturbed Mycoplasma pneumoniae cells to resolve 140 maps that recapitulate bacterial translation during the initiation, elongation, and recycling phases. We visualized multiple transcription-translation complexes, allowing us to propose a threading-based translation reinitiation mechanism and to provide structural evidence for a long-hypothesized supercomplex that coordinates transcription, translation, and membrane attachment. We resolved abundant membrane-associated large ribosomal subunits and suggest that dissociation from membranes depends on the conditional initiation of new translation, consistent with a potentially conserved mechanism in mammalian cells. This work visualizes the multilayered control of bacterial translation and demonstrates the power of in-cell structural biology to investigate regulatory circuits in gene expression.","PeriodicalId":9656,"journal":{"name":"Cell","volume":" ","pages":""},"PeriodicalIF":45.1,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In-cell discovery and characterization of a non-canonical bacterial protein translocation-folding complex. 细胞内非典型细菌蛋白易位折叠复合体的发现和表征。

IF 45.1 1区生物学

Cell Pub Date : 2026-09-25 DOI: 10.1016/j.cell.2026.08.055

Rasmus K Jensen, Liang Xue, Federico Marotta, Joseph C Somody, Joel Selkrig, Swantje Lenz, Juri Rappsilber, Mikhail M Savitski, Jan Kosinski, Athanasios Typas, Maria Zimmermann-Kogadeeva, Peer Bork, Julia Mahamid

{"title":"In-cell discovery and characterization of a non-canonical bacterial protein translocation-folding complex.","authors":"Rasmus K Jensen, Liang Xue, Federico Marotta, Joseph C Somody, Joel Selkrig, Swantje Lenz, Juri Rappsilber, Mikhail M Savitski, Jan Kosinski, Athanasios Typas, Maria Zimmermann-Kogadeeva, Peer Bork, Julia Mahamid","doi":"10.1016/j.cell.2026.08.055","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.055","url":null,"abstract":"Cryo-electron tomography has emerged as a powerful technology for in-cell structural biology and, in combination with breakthroughs in protein structure prediction, offers a unique opportunity for illuminating functions of previously uncharacterized macromolecular complexes. Here, we used the genome-reduced bacterium Mycoplasma pneumoniae as a minimal cell model and determined in-cell maps of an unknown complex located at the cell surface. By combining proteomics, structure prediction, integrative modeling, and bioinformatics, we identified the complex to include the conserved Sec-translocon and an extracellular dome-like structure largely formed by three uncharacterized proteins (Mdps). The Mdps show structural homology to the periplasmic ATP-independent foldase PrsA, with Mdp444 retaining key catalytic residues and activity. Our study provides the first sub-nanometer-resolution maps of the complete bacterial Sec-translocation machinery, depicting its association in SecA-mediated co-translational translocation and its coordination with an extracellular protein-folding system.","PeriodicalId":9656,"journal":{"name":"Cell","volume":" ","pages":""},"PeriodicalIF":45.1,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Shifts in embryonic oxygen levels cue heterochrony in limb initiation 胚胎氧水平的变化提示肢体形成的异时性

IF 64.5 1区生物学

Cell Pub Date : 2026-09-24 DOI: 10.1016/j.cell.2026.08.051

Meng Zhu,ChangHee Lee,Rinaldo Catta-Preta,Clifford J. Tabin

引用次数: 0

A pericyte-to-myofibroblast transition links APOE4 to cerebrovascular degeneration 周细胞到肌成纤维细胞的转变将APOE4与脑血管变性联系起来

IF 64.5 1区生物学

Cell Pub Date : 2026-09-24 DOI: 10.1016/j.cell.2026.08.058

Braxton R. Schuldt,Dominic Haworth-Staines,Andrea Perez-Arevalo,Diede W.M. Broekaart,Ashley Harlock,Leon Wang,Anna Bright,Georgia Gallagher,Grace Rabinowitz,Alison M. Goate,Towfique Raj,Ana C. Pereira,Joel W. Blanchard

{"title":"A pericyte-to-myofibroblast transition links APOE4 to cerebrovascular degeneration","authors":"Braxton R. Schuldt,Dominic Haworth-Staines,Andrea Perez-Arevalo,Diede W.M. Broekaart,Ashley Harlock,Leon Wang,Anna Bright,Georgia Gallagher,Grace Rabinowitz,Alison M. Goate,Towfique Raj,Ana C. Pereira,Joel W. Blanchard","doi":"10.1016/j.cell.2026.08.058","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.058","url":null,"abstract":"Cerebrovascular disease is a major but poorly understood feature of Alzheimer’s disease (AD). The strongest genetic AD risk factor, apolipoprotein E4 (APOE4), is associated with cerebrovascular degeneration, including vascular amyloid deposition and fibrosis. To uncover how APOE4 promotes cerebrovascular pathology, we assembled a single-cell transcriptomic atlas of human brain vasculature. In APOE4 carriers, pericyte abundance was significantly reduced and accompanied by the emergence of a myofibroblast-like cell population co-expressing contraction and extracellular matrix genes. Immunostaining confirmed non-vascular myofibroblasts in APOE4 human and mouse brains. We show that APOE4 pericytes transition into myofibroblasts that secrete fibronectin, which promotes vascular amyloid accumulation. Computational and experimental analyses identified elevated transforming growth factor β (TGF-β) signaling as the driver of this pericyte-to-myofibroblast transition. Inhibition of TGF-β restored pericyte coverage and reduced vascular fibrosis and amyloid to APOE3 levels, revealing a targetable mechanism linking APOE4 to cerebrovascular pathology in AD.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"5 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149027575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Resident tissue macrophages transfer selenium transporter protein to protect pancreatic cancer from ferroptosis 常驻组织巨噬细胞转移硒转运蛋白以保护胰腺癌免于铁凋亡

IF 64.5 1区生物学

Cell Pub Date : 2026-09-24 DOI: 10.1016/j.cell.2026.09.001

Wei Guo,Ziyi Li,Qihan Chen,Garett Dunsmore,Li Jiang,Zhijie An,Ziwen Fu,Yibo Liu,Yufei Shao,Shulin Zhao,Ting Wang,Huan Tang,Chengjian Zhao,Guangyan Zhangyuan,Jia Liu,Pengyi Liu,Zhaoyuan Liu,Jiawen Qian,Shuangyan Zhang,Minmin Shi,Ding He,Yedan Liu,Camille Blériot,Lai Guan Ng,Fan Bai,Lingxi Jiang,Bing Su,Baiyong Shen,Florent Ginhoux

{"title":"Resident tissue macrophages transfer selenium transporter protein to protect pancreatic cancer from ferroptosis","authors":"Wei Guo,Ziyi Li,Qihan Chen,Garett Dunsmore,Li Jiang,Zhijie An,Ziwen Fu,Yibo Liu,Yufei Shao,Shulin Zhao,Ting Wang,Huan Tang,Chengjian Zhao,Guangyan Zhangyuan,Jia Liu,Pengyi Liu,Zhaoyuan Liu,Jiawen Qian,Shuangyan Zhang,Minmin Shi,Ding He,Yedan Liu,Camille Blériot,Lai Guan Ng,Fan Bai,Lingxi Jiang,Bing Su,Baiyong Shen,Florent Ginhoux","doi":"10.1016/j.cell.2026.09.001","DOIUrl":"https://doi.org/10.1016/j.cell.2026.09.001","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC), an aggressive cancer with a poor prognosis, contains resident tissue macrophages (RTMs) present before tumor onset and monocyte-derived macrophages recruited during tumor development, but their distinct roles in supporting tumor progression remain unclear. Combining single-cell profiling, spatial analysis, lineage tracing, RTM depletion, and selenium tracing, we found that RTMs preferentially localize at the tumor border, where they promote epithelial-mesenchymal transition (EMT), tumor growth, and metastasis. Mechanistically, RTMs transfer the selenium transporter Selenop to EMThi tumor cells through LRP8-dependent uptake, increasing tumor-cell selenium availability, limiting lipid peroxidation, and shielding EMThi tumor cells from ferroptosis. RTM-specific Selenop deletion or tumor-cell Lrp8 disruption reduced EMT and tumor progression, whereas ferroptosis inhibition reversed the effect of RTM depletion. Human PDAC showed border-enriched SEPP1+ RTMs near EMThi tumor cells, suggesting a conserved macrophage-derived selenium niche that supports invasive tumor states and highlighting the potential for targeting RTMs or their secretory factors in PDAC.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"56 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149027576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Projection-defined modules reveal mouse motor cortex architecture 投影定义模块揭示小鼠运动皮层结构

IF 64.5 1区生物学

Cell Pub Date : 2026-09-23 DOI: 10.1016/j.cell.2026.08.046

Antonio Falasconi,Harsh Kanodia,Nicholas Lusk,Shenqin Yao,Rui M. Costa,Hongkui Zeng,Silvia Arber

引用次数: 0

CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer CD4 T细胞将KRAS抑制的短暂反应转化为胰腺癌的持久缓解

IF 64.5 1区生物学

Cell Pub Date : 2026-09-23 DOI: 10.1016/j.cell.2026.08.045

Li Qiang,Megan T. Hoffman,Jung-Ho Chun,Brendan Parent,Felix Hambitzer,Frank Peprah,Courtney T.S. Kureshi,Birkley S. Lim,Eugena Chang,Michael J. Walsh,Julissa G. Tello,Tavus Atajanova,Hojeong Shin,Corey Perkins,Rakeeb Kureshi,Yaniris Molina-Aponte,James M. Dougan,Chong Zuo,Lauren Brais,Thomas E. Clancy,James M. Cleary,Jason L. Hornick,Brandon M. Huffman,Joseph D. Mancias,George Molina,Mark Fairweather,Jonathan A. Nowak,Kimberly J. Perez,Douglas A. Rubinson,Sarah Slater,Ritchell van Dams,Jiping Wang,Brian M. Wolpin,Kwok-Kin Wong,Harshabad Singh,Andrew J. Aguirre,David Baker,Michael Dougan,Stephanie K. Dougan

{"title":"CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer","authors":"Li Qiang,Megan T. Hoffman,Jung-Ho Chun,Brendan Parent,Felix Hambitzer,Frank Peprah,Courtney T.S. Kureshi,Birkley S. Lim,Eugena Chang,Michael J. Walsh,Julissa G. Tello,Tavus Atajanova,Hojeong Shin,Corey Perkins,Rakeeb Kureshi,Yaniris Molina-Aponte,James M. Dougan,Chong Zuo,Lauren Brais,Thomas E. Clancy,James M. Cleary,Jason L. Hornick,Brandon M. Huffman,Joseph D. Mancias,George Molina,Mark Fairweather,Jonathan A. Nowak,Kimberly J. Perez,Douglas A. Rubinson,Sarah Slater,Ritchell van Dams,Jiping Wang,Brian M. Wolpin,Kwok-Kin Wong,Harshabad Singh,Andrew J. Aguirre,David Baker,Michael Dougan,Stephanie K. Dougan","doi":"10.1016/j.cell.2026.08.045","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.045","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is refractory to most therapies, including immunotherapies, for which reinvigoration of CD8 T cells through immune checkpoint blockade is insufficient to induce long-term, durable remissions. Direct KRAS inhibitors (KRASi) have shown clinical promise, although acquired resistance is common. We modeled KRASi response and relapse in mice and demonstrated that, unlike chemotherapy or combinations with checkpoint blockade, an interleukin (IL)-21 cytokine mimic (21h10) induced long-term, durable remissions. Its efficacy depends on T helper 1 (Th1)-polarized CD4 T cells, but not on CD8 T cells or tumor cell expression of major histocompatibility complex class I (MHC class I). Specifically, CD4 T cells primed by type 2 conventional dendritic cells (cDC2s) produce interferon γ (IFN-γ), which promotes macrophage-mediated phagocytosis of tumor cells. Ex vivo treatment of human PDAC specimens with 21h10 induces IFN-γ production by infiltrating T cells. Thus, IL-21-elicited CD4 T cells exert antitumor activity in mice and potentially in humans, converting transient responses to KRAS inhibition into durable remissions.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"25 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microbial signaling coordinates group oviposition and predator defense in migratory locusts 微生物信号协调迁徙蝗虫群体产卵和捕食者防御

IF 64.5 1区生物学

Cell Pub Date : 2026-09-23 DOI: 10.1016/j.cell.2026.08.050

Jinxi Yuan,Liping Nie,Lei Shang,Zhongqiang Jia,Shuang Shan,Xiaoqing Zhang,Lingzhi Shi,Yuxiao Zeng,Benke Hong,Xu Cheng,Liwei Zhang,Guirong Wang,Bill S. Hansson,Hetan Chang

{"title":"Microbial signaling coordinates group oviposition and predator defense in migratory locusts","authors":"Jinxi Yuan,Liping Nie,Lei Shang,Zhongqiang Jia,Shuang Shan,Xiaoqing Zhang,Lingzhi Shi,Yuxiao Zeng,Benke Hong,Xu Cheng,Liwei Zhang,Guirong Wang,Bill S. Hansson,Hetan Chang","doi":"10.1016/j.cell.2026.08.050","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.050","url":null,"abstract":"Reproductive synchronization is suggested to enhance fitness in many insects, yet the mechanisms enabling such coordination remain unknown. In Locusta migratoria, we identify a microbiota-derived volatile, 2,4,6-trimethylpyridine (2,4,6-TMP) that coordinates communal oviposition in gregarious females while simultaneously deterring egg predators. Eggs laid by gregarious females emit 2,4,6-TMP, which attracts conspecifics by activating the olfactory receptors LmOR34 and LmOR36; disruption of either receptor abolishes attraction and alters oviposition behavior. 2,4,6-TMP is synthesized by the egg-associated bacterium Enterobacter roggenkampii through a lysine degradation pathway. Deletion of lysine decarboxylase abolishes 2,4,6-TMP production and associated behavioral responses. Beyond facilitating reproduction, 2,4,6-TMP repels soil-dwelling predators, including ants, beetles, and potworms. In the ant Solenopsis invicta, avoidance is mediated by the olfactory receptor SinOR43a-1; RNA interference (RNAi) knockdown of this receptor abolishes repellence. Semi-field assays confirm the ecological relevance of 2,4,6-TMP. These findings reveal an egg-associated bacterial signaling mechanism that couples reproductive coordination with predator defense in L. migratoria.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"16 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Direct cell-to-cell transmission of retrotransposons 逆转录转座子的直接细胞间传递

IF 64.5 1区生物学

Cell Pub Date : 2026-09-23 DOI: 10.1016/j.cell.2026.08.047

Maya Voichek,Andreas Bernhard,Lea Lauterjung,Maria Novatchkova,Dominik Handler,Paul Möseneder,Liudmila Protsenko,Baptiste Rafanel,Svetlana Iarovenko,Peter Duchek,Kirsten-André Senti,Julius Brennecke

{"title":"Direct cell-to-cell transmission of retrotransposons","authors":"Maya Voichek,Andreas Bernhard,Lea Lauterjung,Maria Novatchkova,Dominik Handler,Paul Möseneder,Liudmila Protsenko,Baptiste Rafanel,Svetlana Iarovenko,Peter Duchek,Kirsten-André Senti,Julius Brennecke","doi":"10.1016/j.cell.2026.08.047","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.047","url":null,"abstract":"Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of long terminal repeat (LTR) retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, which bears structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions that contain retroviral capsids and establish physical contact with the oocyte membrane. In the absence of sORF2, protrusion formation and soma-to-germline transmission of capsids are abolished. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"21 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Switching of transcriptional control from interferon regulatory factor 2 to interferon regulatory factor 1 drives innate immune cell activation 从干扰素调节因子2到干扰素调节因子1的转录控制转换驱动先天免疫细胞激活

IF 64.5 1区生物学

Cell Pub Date : 2026-09-22 DOI: 10.1016/j.cell.2026.08.049

Cristhian Cadena,Rohit Reja,Emma Bolech,Joshua D. Webster,Vasumathi Kameswaran,Marco de Simone,Cynthia Chen,Jian Jiang,Kathy Hotzel,Christopher Bjornson,Kamela Alegre,Zhenyu Tan,Heidi J. Elsaesser,Raymond Newland,Ryan Kelly,Spyros Darmanis,Bence Daniel,David G. Brooks,Ishan Deshpande,Kim Newton,Nobuhiko Kayagaki,Vishva M. Dixit

{"title":"Switching of transcriptional control from interferon regulatory factor 2 to interferon regulatory factor 1 drives innate immune cell activation","authors":"Cristhian Cadena,Rohit Reja,Emma Bolech,Joshua D. Webster,Vasumathi Kameswaran,Marco de Simone,Cynthia Chen,Jian Jiang,Kathy Hotzel,Christopher Bjornson,Kamela Alegre,Zhenyu Tan,Heidi J. Elsaesser,Raymond Newland,Ryan Kelly,Spyros Darmanis,Bence Daniel,David G. Brooks,Ishan Deshpande,Kim Newton,Nobuhiko Kayagaki,Vishva M. Dixit","doi":"10.1016/j.cell.2026.08.049","DOIUrl":"https://doi.org/10.1016/j.cell.2026.08.049","url":null,"abstract":"Interferon regulatory factor 2 (IRF2) is a transcription factor that prevents skin inflammation in mice and humans but, paradoxically, promotes pyroptosis by upregulating gasdermin D. How IRF2 activates some proinflammatory genes but suppresses inflammation is unclear. We show that skin inflammation in Irf2-deficient mice is driven by IRF1 activation of interferon-stimulated genes (ISGs). Chromatin profiling reveals that IRF1 and IRF2 occupy the same ISG regulatory sites, but as a weaker transcriptional activator, IRF2 limits ISG transcription by IRF1. Toll-like receptor (TLR) signaling favors IRF1-driven transcription by inducing Irf1. In addition, IRF1 recruits the ubiquitin ligase SPOP to ISG sites, resulting in proteasomal degradation of IRF2. This shift from IRF2 to IRF1 occupancy enhances ISG transcription. Collectively, these findings define a hierarchical transcriptional circuit in which IRF2 limits IRF1 activity under homeostatic conditions but is displaced during an immune response, allowing IRF1-dependent gene programs central to innate immunity and autoinflammation.","PeriodicalId":9656,"journal":{"name":"Cell","volume":"47 1","pages":""},"PeriodicalIF":64.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149013623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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