Science Immunology最新文献

{"title":"Architects of immunity: How dendritic cells shape CD8+ T cell fate in cancer","authors":"Vidit Bhandarkar,&nbsp;Teresa Dinter,&nbsp;Stefani Spranger","doi":"10.1126/sciimmunol.adf4726","DOIUrl":"10.1126/sciimmunol.adf4726","url":null,"abstract":"<div >Immune responses against cancer are dominated by T cell exhaustion and dysfunction. Recent advances have underscored the critical role of early priming interactions in establishing T cell fates. In this review, we explore the importance of dendritic cell (DC) signals in specifying CD8⁺ T cell fates in cancer, drawing on insights from acute and chronic viral infection models. We highlight the role of DCs in lymph nodes and tumors in maintaining stem-like CD8⁺ T cells, which are critical for durable antitumor immune responses. Understanding how CD8⁺ T cell fates are determined will enable the rational design of immunotherapies, particularly therapeutic cancer vaccines, that can modulate DC–T cell interactions to generate beneficial CD8⁺ T cell fates.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142987475","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":"Obesity reshapes regulatory T cells in the visceral adipose tissue by disrupting cellular cholesterol homeostasis","authors":"Cody Elkins,&nbsp;Chengyu Ye,&nbsp;Pulavendran Sivasami,&nbsp;Roy Mulpur,&nbsp;Pamela P. Diaz-Saldana,&nbsp;Amy Peng,&nbsp;Miaoer Xu,&nbsp;Yeun-po Chiang,&nbsp;Samara Moll,&nbsp;Dormarie E. Rivera-Rodriguez,&nbsp;Luisa Cervantes-Barragan,&nbsp;Tuoqi Wu,&nbsp;Byron B. Au-Yeung,&nbsp;Christopher D. Scharer,&nbsp;Mandy L. Ford,&nbsp;Haydn Kissick,&nbsp;Chaoran Li","doi":"10.1126/sciimmunol.adl4909","DOIUrl":"10.1126/sciimmunol.adl4909","url":null,"abstract":"<div >Regulatory T cells (T_regs) accumulate in the visceral adipose tissue (VAT) to maintain systemic metabolic homeostasis but decline during obesity. Here, we explored the metabolic pathways controlling the homeostasis, composition, and function of VAT T_regs under normal and high-fat diet feeding conditions. We found that cholesterol metabolism was specifically up-regulated in ST2^hi VAT T_reg subsets. T_reg-specific deletion of <i>Srebf2</i>, the master regulator of cholesterol homeostasis, selectively reduced ST2^hi VAT T_regs, increasing VAT inflammation and insulin resistance. Single-cell RNA/T cell receptor (TCR) sequencing revealed a specific loss and reduced clonal expansion of ST2^hi VAT T_reg subsets after <i>Srebf2</i> deletion. <i>Srebf2</i>-mediated cholesterol homeostasis potentiated strong TCR signaling, which preferentially promoted ST2^hi VAT T_reg accumulation. However, long-term high-fat diet feeding disrupted VAT T_reg cholesterol homeostasis and impaired clonal expansion of the ST2^hi subset. Restoring T_reg cholesterol homeostasis rescued VAT T_reg accumulation in obese mice, suggesting that modulation of cholesterol homeostasis could be a promising strategy for T_reg-targeted therapies in obesity-associated metabolic diseases.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142939926","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":"TSLP acts on regulatory T cells to maintain their identity and limit allergic inflammation","authors":"Rama K. Gurram,&nbsp;Peng Li,&nbsp;Jangsuk Oh,&nbsp;Xi Chen,&nbsp;Rosanne Spolski,&nbsp;Xianglan Yao,&nbsp;Jian-Xin Lin,&nbsp;Suyasha Roy,&nbsp;Matthew J. Liao,&nbsp;Chengyu Liu,&nbsp;Zu-Xi Yu,&nbsp;Stewart J. Levine,&nbsp;Jinfang Zhu,&nbsp;Warren J. Leonard","doi":"10.1126/sciimmunol.adk0073","DOIUrl":"10.1126/sciimmunol.adk0073","url":null,"abstract":"<div >Thymic stromal lymphopoietin (TSLP) is a type I cytokine that promotes allergic responses and mediates type 2 immunity. A balance between effector T cells (T_effs), which drive the immune response, and regulatory T cells (T_regs), which suppress the response, is required for proper immune homeostasis. Here, we report that TSLP differentially acts on T_effs versus T_regs to balance type 2 immunity. As expected, deletion of TSLP receptor (TSLPR) on all T cells (<i>Cd4</i>^Cre<i>Crlf2</i>^fl/fl mice) resulted in lower numbers of T helper 2 (T_H2) cells and diminished ovalbumin-induced airway inflammation, but selective deletion of TSLPR on T_regs (<i>Foxp3</i>^{<i>YFP</i>-Cre/Y}<i>Crlf2</i>^fl/fl mice) resulted in increased interleukin-5 (IL-5)– and IL-13–secreting T_H2 cells and lung eosinophilia. Moreover, TSLP augmented the expression of factors that stabilize T_regs. During type 2 immune responses, TSLPR-deficient T_regs acquired T_H2-like properties, with augmented GATA3 expression and secretion of IL-13. TSLP not only is a driver of T_H2 effector cells but also acts in a negative feedback loop, thus promoting the ability of T_regs to limit allergic inflammation.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142939924","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":"Multiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature","authors":"Marita Bosticardo,&nbsp;Kerry Dobbs,&nbsp;Ottavia M. Delmonte,&nbsp;Andrew J. Martins,&nbsp;Francesca Pala,&nbsp;Tomoki Kawai,&nbsp;Heather Kenney,&nbsp;Gloria Magro,&nbsp;Lindsey B. Rosen,&nbsp;Yasuhiro Yamazaki,&nbsp;Hsin-Hui Yu,&nbsp;Enrica Calzoni,&nbsp;Yu Nee Lee,&nbsp;Can Liu,&nbsp;Jennifer Stoddard,&nbsp;Julie Niemela,&nbsp;Danielle Fink,&nbsp;Riccardo Castagnoli,&nbsp;Meredith Ramba,&nbsp;Aristine Cheng,&nbsp;Deanna Riley,&nbsp;Vasileios Oikonomou,&nbsp;Elana Shaw,&nbsp;Brahim Belaid,&nbsp;Sevgi Keles,&nbsp;Waleed Al-Herz,&nbsp;Caterina Cancrini,&nbsp;Cristina Cifaldi,&nbsp;Safa Baris,&nbsp;Svetlana Sharapova,&nbsp;Catharina Schuetz,&nbsp;Andrew R. Gennery,&nbsp;Alexandra F. Freeman,&nbsp;Raz Somech,&nbsp;Sharon Choo,&nbsp;Silvia C. Giliani,&nbsp;Tayfun Güngör,&nbsp;Daniel Drozdov,&nbsp;Isabelle Meyts,&nbsp;Despina Moshous,&nbsp;Benedicte Neven,&nbsp;Roshini S. Abraham,&nbsp;Aisha El-Marsafy,&nbsp;Maria Kanariou,&nbsp;Alejandra King,&nbsp;Francesco Licciardi,&nbsp;Mario E. Cruz-Muñoz,&nbsp;Paolo Palma,&nbsp;Cecilia Poli,&nbsp;Mehdi Adeli,&nbsp;Mattia Algeri,&nbsp;Fayhan J. Alroqi,&nbsp;Paul Bastard,&nbsp;Jenna R. E. Bergerson,&nbsp;Claire Booth,&nbsp;Ana Brett,&nbsp;Siobhan O. Burns,&nbsp;Manish J. Butte,&nbsp;Nurcicek Padem,&nbsp;M. Teresa de la Morena,&nbsp;Ghassan Dbaibo,&nbsp;Suk See de Ravin,&nbsp;Dimana Dimitrova,&nbsp;Reda Djidjik,&nbsp;Mayra B. Dorna,&nbsp;Cullen M. Dutmer,&nbsp;Reem Elfeky,&nbsp;Fabio Facchetti,&nbsp;Ramsay L. Fuleihan,&nbsp;Raif S. Geha,&nbsp;Luis I. Gonzalez-Granado,&nbsp;Liis Haljasmägi,&nbsp;Hanadys Ale,&nbsp;Anthony Hayward,&nbsp;Anna M. Hifanova,&nbsp;Winnie Ip,&nbsp;Blanka Kaplan,&nbsp;Neena Kapoor,&nbsp;Elif Karakoc-Aydiner,&nbsp;Jaanika Kärner,&nbsp;Michael D. Keller,&nbsp;Blachy J. Dávila Saldaña,&nbsp;Ayça Kiykim,&nbsp;Taco W. Kuijpers,&nbsp;Elena E. Kuznetsova,&nbsp;Elena A. Latysheva,&nbsp;Jennifer W. Leiding,&nbsp;Franco Locatelli,&nbsp;Guisela Alva-Lozada,&nbsp;Christine McCusker,&nbsp;Fatih Celmeli,&nbsp;Megan Morsheimer,&nbsp;Ahmet Ozen,&nbsp;Nima Parvaneh,&nbsp;Srdjan Pasic,&nbsp;Alessandro Plebani,&nbsp;Kahn Preece,&nbsp;Susan Prockop,&nbsp;Inga S. Sakovich,&nbsp;Elena E. Starkova,&nbsp;Troy Torgerson,&nbsp;James Verbsky,&nbsp;Jolan E. Walter,&nbsp;Brant Ward,&nbsp;Elizabeth L. Wisner,&nbsp;Deborah Draper,&nbsp;Katherine Myint-Hpu,&nbsp;Pooi M. Truong,&nbsp;Michail S. Lionakis,&nbsp;Morgan B. Similuk,&nbsp;Centralized Sequencing Program Group§§,&nbsp;Magdalena A. Walkiewicz,&nbsp;Amy Klion,&nbsp;Steven M. Holland,&nbsp;Cihan Oguz,&nbsp;Dusan Bogunovic,&nbsp;Kai Kisand,&nbsp;Helen C. Su,&nbsp;John S. Tsang,&nbsp;Douglas Kuhns,&nbsp;Anna Villa,&nbsp;Sergio D. Rosenzweig,&nbsp;Stefania Pittaluga,&nbsp;Luigi D. Notarangelo","doi":"10.1126/sciimmunol.adq1697","DOIUrl":"10.1126/sciimmunol.adq1697","url":null,"abstract":"<div >Human recombination-activating gene (RAG) deficiency can manifest with distinct clinical and immunological phenotypes. By applying a multiomics approach to a large group of <i>RAG</i>-mutated patients, we aimed at characterizing the immunopathology associated with each phenotype. Although defective T and B cell development is common to all phenotypes, patients with hypomorphic <i>RAG</i> variants can generate T and B cells with signatures of immune dysregulation and produce autoantibodies to a broad range of self-antigens, including type I interferons. T helper 2 (T_H2) cell skewing and a prominent inflammatory signature characterize Omenn syndrome, whereas more hypomorphic forms of RAG deficiency are associated with a type 1 immune profile both in blood and tissues. We used cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) analysis to define the cell lineage–specific contribution to the immunopathology of the distinct RAG phenotypes. These insights may help improve the diagnosis and clinical management of the various forms of the disease.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adq1697","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056081","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":"Suppression of thrombospondin-1–mediated inflammaging prolongs hematopoietic health span","authors":"Pradeep Ramalingam,&nbsp;Michael C. Gutkin,&nbsp;Michael G. Poulos,&nbsp;Agatha Winiarski,&nbsp;Arianna Smith,&nbsp;Cody Carter,&nbsp;Chelsea Doughty,&nbsp;Taylor Tillery,&nbsp;David Redmond,&nbsp;Ana G. Freire,&nbsp;Jason M. Butler","doi":"10.1126/sciimmunol.ads1556","DOIUrl":"10.1126/sciimmunol.ads1556","url":null,"abstract":"<div >Chronic low-grade inflammation observed in older adults, termed inflammaging, is a common feature underlying a multitude of aging-associated maladies including a decline in hematopoietic activity. However, whether suppression of inflammaging can preserve hematopoietic health span remains unclear, in part because of a lack of tools to measure inflammaging within hematopoietic stem cells (HSCs). Here, we identify thrombospondin-1 (Thbs1) as an essential regulator of inflammaging within HSCs. We describe a transcriptomics-based approach for measuring inflammaging within stem cells and demonstrate that deletion of <i>Thbs1</i> is sufficient to prevent HSC inflammaging. Our results demonstrate that suppression of HSC inflammaging prevents aging-associated defects in hematopoietic activity including loss of HSC self-renewal, myeloid-biased HSC differentiation, and anemia. Our findings indicate that suppression of HSC inflammaging may also prolong overall systemic health span.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads1556","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142917895","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":"SNIPR alert! Making T cells more precise killers","authors":"Jonathan Chuck,&nbsp;Laura A. Solt","doi":"10.1126/sciimmunol.adv4911","DOIUrl":"10.1126/sciimmunol.adv4911","url":null,"abstract":"<div >A cell engineering approach demonstrates that precise regulation of cell signaling can be achieved using both endogenous and synthetic ligands.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927977","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":"NEK7 phosphorylation amplifies NLRP3 inflammasome activation downstream of potassium efflux and gasdermin D","authors":"Jie Xu,&nbsp;Lingzhi Zhang,&nbsp;Yanhui Duan,&nbsp;Fangyuan Sun,&nbsp;Nouha Odeh,&nbsp;Yuan He,&nbsp;Gabriel Núñez","doi":"10.1126/sciimmunol.adl2993","DOIUrl":"10.1126/sciimmunol.adl2993","url":null,"abstract":"<div >The NLRP3 inflammasome plays a critical role in innate immunity and inflammatory diseases. NIMA-related kinase 7 (NEK7) is essential for inflammasome activation, and its interaction with NLRP3 is enhanced by K⁺ efflux. However, the mechanism by which K⁺ efflux promotes this interaction remains unknown. Here, we show that NEK7 is rapidly phosphorylated at threonine-190/191 by JNK1 downstream of K⁺ efflux and gasdermin D (GSDMD) after NLRP3 activation. NEK7 phosphorylation enhances the binding between NEK7 and NLRP3, which further promotes inflammasome assembly and activation. Mutant mice and macrophages in which Thr¹⁹⁰ and Thr¹⁹¹ of Nek7 were replaced by valine exhibited impaired NEK7 phosphorylation, NLRP3 inflammasome activation, and IL-1β secretion. Thus, NEK7 phosphorylation is an important event that acts downstream of K⁺ efflux and GSDMD to further enhance NLRP3 inflammasome activation.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142917751","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":"Molecular scalpels dissect new GluN1 hot spots in anti–NMDA receptor encephalitis","authors":"Marianna Spatola,&nbsp;Josep Dalmau","doi":"10.1126/sciimmunol.adv4913","DOIUrl":"10.1126/sciimmunol.adv4913","url":null,"abstract":"<div >Patient-derived NMDAR mAbs combined with single-particle cryo-electron microscopy reveal multiple GluN1 epitopes and distinct functional effects.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927976","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":"Functional differences between rodent and human PD-1 linked to evolutionary divergence","authors":"Takeya Masubuchi,&nbsp;Lin Chen,&nbsp;Nimi Marcel,&nbsp;George A. Wen,&nbsp;Christine Caron,&nbsp;Jibin Zhang,&nbsp;Yunlong Zhao,&nbsp;Gerald P. Morris,&nbsp;Xu Chen,&nbsp;Stephen M. Hedrick,&nbsp;Li-Fan Lu,&nbsp;Chuan Wu,&nbsp;Zhengting Zou,&nbsp;Jack D. Bui,&nbsp;Enfu Hui","doi":"10.1126/sciimmunol.ads6295","DOIUrl":"10.1126/sciimmunol.ads6295","url":null,"abstract":"<div >Mechanistic understanding of the inhibitory immunoreceptor PD-1 is largely based on mouse models, but human and mouse PD-1 share only 59.6% amino acid identity. Here, we found that human PD-1 is more inhibitory than mouse PD-1, owing to stronger interactions with the ligands PD-L1 and PD-L2 and more efficient recruitment of the effector phosphatase Shp2. In a mouse melanoma model with adoptively transferred T cells, humanization of a PD-1 intracellular domain disrupted the antitumor activity of CD8⁺ T cells and increased the magnitude of anti–PD-1 response. We identified a motif highly conserved across vertebrate PD-1 orthologs, absent in rodents, as a key determinant for differential Shp2 recruitment. Evolutionary analysis suggested that PD-1 underwent a rodent lineage–specific functional attenuation during evolution. Together, our study uncovers species-specific features of the PD-1 pathway, with implications for PD-1 evolution and differential anti–PD-(L)1 responses in mouse models and human patients.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 103","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142917894","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":"Extrasinusoidal macrophages are a distinct subset of immunologically active dural macrophages","authors":"Lukas Amann,&nbsp;Amelie Fell,&nbsp;Gianni Monaco,&nbsp;Roman Sankowski,&nbsp;Huang Zie Quann Wu,&nbsp;Marta Joana Costa Jordão,&nbsp;Katharina Borst,&nbsp;Maximilian Fliegauf,&nbsp;Takahiro Masuda,&nbsp;Alberto Ardura-Fabregat,&nbsp;Neil Paterson,&nbsp;Elisa Nent,&nbsp;James Cook,&nbsp;Ori Staszewski,&nbsp;Omar Mossad,&nbsp;Thorsten Falk,&nbsp;Antoine Louveau,&nbsp;Igor Smirnov,&nbsp;Jonathan Kipnis,&nbsp;Tim Lämmermann,&nbsp;Marco Prinz","doi":"10.1126/sciimmunol.adh1129","DOIUrl":"10.1126/sciimmunol.adh1129","url":null,"abstract":"<div >Although macrophages in the meningeal compartments of the central nervous system (CNS) have been comprehensively characterized under steady state, studying their contribution to physiological and pathological processes has been hindered by the lack of specific targeting tools in vivo. Recent findings have shown that the dural sinus and its adjacent lymphatic vessels act as a neuroimmune interface. However, the cellular and functional heterogeneity of extrasinusoidal dural macrophages outside this immune hub is not fully understood. Therefore, we comprehensively characterized these cells using single-cell transcriptomics, fate mapping, confocal imaging, clonal analysis, and transgenic mouse lines. Extrasinusoidal dural macrophages were distinct from leptomeningeal and CNS parenchymal macrophages in terms of their origin, expansion kinetics, and transcriptional profiles. During autoimmune neuroinflammation, extrasinusoidal dural macrophages performed efferocytosis of apoptotic granulocytes. Our results highlight a previously unappreciated myeloid cell diversity and provide insights into the brain’s innate immune system.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 102","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142867118","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}