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CD21 primes extrafollicular differentiation of autoreactive B cells in a TLR7-driven lupus model 在tlr7驱动的狼疮模型中,CD21启动自身反应性B细胞的滤泡外分化
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-14 DOI: 10.1126/sciimmunol.ads8226
Danni Y. Zhu, Daniel P. Maurer, Carlos Castrillon, Yixiang Deng, Faez A. N. Mohamed, Minghe Ma, David Tang, Jessica Min-Debartolo, Nathan Higginson-Scott, Janet Buhlmann, Aaron G. Schmidt, Daniel Lingwood, Michael C. Carroll
The extrafollicular (EF) B cell differentiation pathway has emerged as a prominent source of autoantibody-secreting cells (ASCs) in systemic lupus erythematosus (SLE). CD21loCD11c+ B cells are associated with aging, infection, and autoimmunity. They are key contributors to EF ASCs, yet their developmental trajectory and receptor programming are unclear. To study EF mechanics of autoreactive B cells, we adoptively transferred naïve B cell populations into 564Igi mice, which act as an autoreactive host enriched for autoantigens and T cell help. Time-resolved analyses revealed a Toll-like receptor 7 (TLR7)–dependent early escape of peripheral tolerance and a pre–ASC division program. We identified naïve-derived CD21lo cells as precursors of EF ASCs exhibiting elevated reliance on TLR7. Repertoire analysis delineated protoautoreactive B cell selection and receptor evolution toward self-reactivity. Continuous complement receptor 2 (CR2/CD21)–complement C3d and CD21–complement iC3b engagement triggered receptor down-regulation before proliferation. We reveal CD21 as an initiator of TLR7-dependent autoimmune EF proliferation and target for suppressing autoreactivity.
在系统性红斑狼疮(SLE)中,滤泡外(EF) B细胞分化途径已成为自身抗体分泌细胞(ASCs)的重要来源。CD21 - CD11c + B细胞与衰老、感染和自身免疫有关。它们是EF ASCs的关键贡献者,但它们的发育轨迹和受体编程尚不清楚。为了研究自身反应性B细胞的EF机制,我们过继性地将naïve B细胞群转移到564Igi小鼠中,该小鼠作为富含自身抗原和T细胞帮助的自身反应性宿主。时间分辨分析显示toll样受体7 (TLR7)依赖性外周耐受性的早期逃逸和asc前分裂程序。我们发现naïve-derived CD21细胞是EF ASCs的前体,表现出对TLR7的高度依赖。保留库分析描述了原自身反应性B细胞的选择和受体向自我反应性的进化。持续补体受体2 (CR2/CD21) -补体C3d和CD21 -补体iC3b结合触发受体在增殖前下调。我们发现CD21是tlr7依赖性自身免疫性EF增殖的启动器和抑制自身反应性的靶标。
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引用次数: 0
An islet-resident macrophage antioxidant program preserves β cell physiology 胰岛巨噬细胞抗氧化程序保留β细胞的生理机能
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-14 DOI: 10.1126/sciimmunol.adz5181
Amélie Grosjean, Aude Jalon, Claire Leveau, Marc Diedisheim, David Alejandro Bejarano, Joyceline Cuenco, Kevin Mulder, Zhaoyuan Liu, Audrey Le Guernic, Marie-Laure Island, Jarne Walkiers, Gamze Ates, Clément Materne, Andreia Goncalves, Ivan Nemazanyy, Laura G. Baudrin, Sylvain Baulande, Martine Ropert, Jean-François Gautier, Ahmed Hamaï, Andreas Schlitzer, Florent Ginhoux, Ann Massie, Nicolas Venteclef, Elise Dalmas
Pancreatic islet-resident macrophages (IRMs) display an activated phenotype and contribute to islet development and remodeling, yet their origin, heterogeneity, and functional roles remain poorly understood. Using complementary fate-mapping systems, we show that, in adult mice, around half of IRMs originate from circulating monocytes and undergo minimal turnover. Integrated multiple single-cell RNA sequencing analyses of mouse and human islets identified four major IRM cell states that collectively reveal their inflammatory and metabolic activation. Among these, a transcriptional program driven by the cystine-glutamate antiporter SLC7A11 and enriched in CD9high IRMs was associated with enhanced antioxidant defense, mitochondrial activity, and iron-lipid metabolic pathways. We found that Slc7a11-expressing IRMs preserve β cell redox homeostasis and insulin secretion, both at baseline and under stress. These findings position IRMs as specialized immune sentinels in the endocrine pancreas and identify SLC7A11 as a key macrophage-intrinsic safeguard against oxidative stress, with broad implications for islet resilience and metabolic health.
胰岛常驻巨噬细胞(IRMs)表现出一种活化的表型,并有助于胰岛的发育和重塑,但它们的起源、异质性和功能作用仍然知之甚少。利用互补的命运定位系统,我们发现,在成年小鼠中,大约一半的irm来自循环单核细胞,并且经历最小的周转。对小鼠和人类胰岛的综合多单细胞RNA测序分析确定了四种主要的IRM细胞状态,这些细胞状态共同揭示了它们的炎症和代谢激活。其中,由胱氨酸-谷氨酸反转运蛋白SLC7A11驱动并富集CD9高IRMs的转录程序与增强的抗氧化防御、线粒体活性和铁脂代谢途径相关。我们发现,在基线和应激条件下,表达Slc7a11的IRMs都能保持β细胞氧化还原稳态和胰岛素分泌。这些发现将IRMs定位为内分泌胰腺中的特殊免疫哨兵,并确定SLC7A11是巨噬细胞抵抗氧化应激的关键内在保障,对胰岛恢复能力和代谢健康具有广泛意义。
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引用次数: 0
Two of a kind, one with MS: Gut microbes tip the balance 两种类型,一种是多发性硬化症:肠道微生物打破了平衡
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-07 DOI: 10.1126/sciimmunol.aed4910
Kevin Champagne-Jorgensen, Jennifer L. Gommerman
An MS twin study links ileal Lachnospiraceae to spontaneous CNS autoimmunity in mice receiving a human microbiome transplant.
一项MS双胞胎研究将回肠毛缕菌科与接受人类微生物组移植的小鼠自发性中枢神经系统自身免疫联系起来。
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引用次数: 0
Characterization of the mammalian prodefinitive angio-hematopoietic lineage 哺乳动物前驱血管-造血谱系的表征
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-07 DOI: 10.1126/sciimmunol.adt6616
Tomi Lazarov, Pierre-Louis Loyher, Hairu Yang, Zi-Ning Choo, Zihou Deng, Sonja Nowotschin, Ying-Yi Kuo, Ting Zhou, Araitz Alberdi-Gonzalez, Ralf Stumm, Elvira Mass, Elisa Gomez Perdiguero, Anna-Katerina Hadjantonakis, Frederic Geissmann
Mammalian hematopoietic cells arise from mesodermal progenitors in a close developmental relationship with endothelium and along three distinct cell lineages known as primitive, prodefinitive, and definitive hematopoiesis. However, the developmental hierarchies between early mesodermal progenitors, endothelium, and blood cell lineages are incompletely understood. Here, fate-mapping, cloning, and genetic experiments identified a population of KDR+CXCR4+ prodefinitive angio-hematopoietic progenitors (PDAPs) in murine primitive streak stage mesoderm and human induced pluripotent stem cell (hiPSC) cultures. PDAPs gave rise to yolk sac (YS) and rostral (cephalic) endothelial cells and RUNX1-dependent prodefinitive hematopoietic cells, including erythro-myeloid progenitors (EMPs) and tissue macrophages, via NOTCH1-independent hemogenic endothelial cells. Notably, PDAPs did not give rise to primitive erythropoiesis or to caudal endothelium and definitive hematopoiesis. These results identify a previously unrecognized layer of lineage segregation in early mammalian mesoderm that characterizes the prodefinitive angio-hematopoietic lineage and the origin of tissue macrophages and rostral blood vessels that may be of interest for pathophysiology and cell-based therapy efforts.
哺乳动物造血细胞起源于中胚层祖细胞,与内皮细胞有着密切的发育关系,并沿着三种不同的细胞系发展,即原始造血、终代造血和终代造血。然而,早期中胚层祖细胞、内皮细胞和血细胞谱系之间的发育等级尚不完全清楚。在这里,命运定位、克隆和遗传实验在小鼠原始条纹期中胚层和人诱导多能干细胞(hiPSC)培养中鉴定了KDR + CXCR4 +前代血管造血祖细胞(ppdaps)群体。pdap通过不依赖notch1的造血内皮细胞产生卵黄囊(YS)和吻侧(头侧)内皮细胞和依赖runx1的前代造血细胞,包括红髓祖细胞(EMPs)和组织巨噬细胞。值得注意的是,pdap不能引起原始红细胞生成,也不能引起尾端内皮和最终造血。这些结果确定了早期哺乳动物中胚层中一个以前未被认识的谱系分离层,它表征了前代血管造血谱系和组织巨噬细胞和吻侧血管的起源,这可能对病理生理学和细胞基础治疗工作感兴趣。
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引用次数: 0
B cells and dengue: A cat-and-mouse game B细胞和登革热:猫捉老鼠的游戏
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-07 DOI: 10.1126/sciimmunol.aed4909
Kritika Dixit, David R. Martinez
Repeated dengue infections elicit broadly neutralizing antibodies that are protective against severe disease.
反复的登革热感染引发广泛的中和抗体,对严重疾病具有保护作用。
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引用次数: 0
B cells targeting parasites capture spatially linked antigens to secure T cell help 靶向寄生虫的B细胞捕获空间连接抗原以获得T细胞的帮助
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-07 DOI: 10.1126/sciimmunol.adw0415
Xin Gao, Hayley A. McNamara, Jiwon Lee, Adrian F. Lo, Deepyan Chatterjee, Dominik Spensberger, Daniel Fernandez-Ruiz, Kevin Walz, Ke Wang, Hannah G. Kelly, Kai Pohl, Patricia E. Carreira, Andrea Do, Le Xiong, Lynette Beattie, Alexandra J. Spencer, Daniel H. D. Gray, Friedrich Frischknecht, Melanie Rug, Ian A. Cockburn
T cell–dependent antibody responses have been well studied in the context of small proteins and viruses. However, how B cells acquire and process antigens from large pathogens such as parasites remains poorly understood. Here, using Plasmodium sporozoites (SPZs) as a model, we investigated the formation of protective antibody responses against the circumsporozoite protein (CSP), a vaccine antigen expressed on the surfaces of SPZs. CSP-specific B cells took up CSP and bystander surface antigens during SPZ immunization and could obtain both intramolecular and intermolecular T cell help. Furthermore, prior exposure to blood-stage parasites—which predominantly share internal but not surface antigens with SPZs—can hinder the generation of anti-CSP antibodies. Thus, spatial relationships between the target antigens can affect CD4 T cell help to B cells. These data show how B cells obtain antigen for presentation to T cells and why malaria-exposed individuals have impaired antibody responses to CSP.
T细胞依赖性抗体反应已经在小蛋白和病毒的背景下得到了很好的研究。然而,B细胞如何从大型病原体(如寄生虫)获取和处理抗原仍然知之甚少。本文以疟原虫孢子子(SPZs)为模型,研究了针对环孢子子蛋白(CSP)的保护性抗体反应的形成。环孢子子蛋白是一种表达在SPZs表面的疫苗抗原。在SPZ免疫过程中,CSP特异性B细胞吸收CSP和旁观者表面抗原,并获得分子内和分子间T细胞的帮助。此外,先前暴露于血期寄生虫(主要与spz共享内部而非表面抗原)可以阻碍抗csp抗体的产生。因此,靶抗原之间的空间关系可以影响CD4 T细胞对B细胞的帮助。这些数据显示了B细胞如何获得抗原以提交给T细胞,以及为什么暴露于疟疾的个体对CSP的抗体反应受损。
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引用次数: 0
TH17 cells converted into exTH17 cells sustain rheumatoid-like IL-17–independent inflammatory arthritis th17细胞转化为exT h17细胞维持类风湿样il -17不依赖型炎性关节炎
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-11-07 DOI: 10.1126/sciimmunol.adm7800
Martina Zoccheddu, Kensuke Suga, Amara Seng, Mattias N. D. Svensson, Paramita Dutta, Sanaz Panahandeh, Hadijat-Kubura Moradeke Makinde, Myungja Ro, Yizhou Wang, Hyobin Kim, Zbigniew Mikulski, Katarzyna Dobaczewska, Francesca Ingegnoli, Ruth Minsha, John F. Seagrist, Mary Carns, Kathleen Aren, Salina Dominguez, Mohammad Daud Khan, Angela Denn, Roberto Caporali, Pietro Simone Randelli, David A. McBride, Arthur M. Mandelin II, Carla Marie Cuda, Zhiping Paul Wang, Jason H. Moore, Nisarg J. Shah, Kyoung Jae Won, Deborah R. Winter, Ferhat Ay, Harris Perlman, Nunzio Bottini
T helper 17 (TH17) cells are found in the periphery and synovium of patients with rheumatoid arthritis (RA); however, IL-17–targeted interventions have limited efficacy in established RA. Inflammation can induce TH17 cell transdifferentiation into IL-17–negative exTH17 cells, but the role of exTH17 cells in arthritis is unknown. We performed TH17 cell lineage tracing in the SKG mouse model of RA. In arthritic mice, synovial TH17 cells transdifferentiate into CD44+ exTH17 cells, which are more arthritogenic and sustain inflammation that is IL-17 independent. The exTH17 cell gene signature includes up-regulation of CD44 and sphingosine-1-phosphate receptor 4 (S1PR4) and correlates with the profile of human RA synovial CD4+ T cells. We demonstrate that cross-talk between TH17 cells and fibroblast-like synoviocytes (FLSs) via S1P promotes TH17-exTH17 cell conversion. CD44 is necessary for exTH17 cell–mediated arthritis. Our study suggests that FLS expansion during RA progression promotes TH17-exTH17 cell conversion. These results could potentially enable RA precision therapy.
类风湿关节炎(RA)患者的外周和滑膜中发现T辅助17 (ht17)细胞;然而,针对il -17的干预措施对已建立的RA的疗效有限。炎症可诱导T H 17细胞转分化为il -17阴性的exT H 17细胞,但exT H 17细胞在关节炎中的作用尚不清楚。我们在类风湿关节炎的SKG小鼠模型中进行了ht17细胞谱系追踪。在关节炎小鼠中,滑膜ht17细胞转分化为CD44 + exT h17细胞,后者更具有关节炎性,并维持不依赖IL-17的炎症。exT h17细胞基因特征包括CD44和鞘氨醇-1-磷酸受体4 (S1PR4)的上调,并与人RA滑膜CD4 + T细胞的谱相关。我们证明了th17细胞和成纤维细胞样滑膜细胞(FLSs)之间通过S1P的相互作用促进了th17 - ext h17细胞的转化。CD44对于exT h17细胞介导的关节炎是必需的。我们的研究表明,在RA进展过程中FLS的扩增促进了ht17 - ext h17细胞的转化。这些结果可能使RA精确治疗成为可能。
{"title":"TH17 cells converted into exTH17 cells sustain rheumatoid-like IL-17–independent inflammatory arthritis","authors":"Martina Zoccheddu,&nbsp;Kensuke Suga,&nbsp;Amara Seng,&nbsp;Mattias N. D. Svensson,&nbsp;Paramita Dutta,&nbsp;Sanaz Panahandeh,&nbsp;Hadijat-Kubura Moradeke Makinde,&nbsp;Myungja Ro,&nbsp;Yizhou Wang,&nbsp;Hyobin Kim,&nbsp;Zbigniew Mikulski,&nbsp;Katarzyna Dobaczewska,&nbsp;Francesca Ingegnoli,&nbsp;Ruth Minsha,&nbsp;John F. Seagrist,&nbsp;Mary Carns,&nbsp;Kathleen Aren,&nbsp;Salina Dominguez,&nbsp;Mohammad Daud Khan,&nbsp;Angela Denn,&nbsp;Roberto Caporali,&nbsp;Pietro Simone Randelli,&nbsp;David A. McBride,&nbsp;Arthur M. Mandelin II,&nbsp;Carla Marie Cuda,&nbsp;Zhiping Paul Wang,&nbsp;Jason H. Moore,&nbsp;Nisarg J. Shah,&nbsp;Kyoung Jae Won,&nbsp;Deborah R. Winter,&nbsp;Ferhat Ay,&nbsp;Harris Perlman,&nbsp;Nunzio Bottini","doi":"10.1126/sciimmunol.adm7800","DOIUrl":"10.1126/sciimmunol.adm7800","url":null,"abstract":"<div >T helper 17 (T<sub>H</sub>17) cells are found in the periphery and synovium of patients with rheumatoid arthritis (RA); however, IL-17–targeted interventions have limited efficacy in established RA. Inflammation can induce T<sub>H</sub>17 cell transdifferentiation into IL-17–negative exT<sub>H</sub>17 cells, but the role of exT<sub>H</sub>17 cells in arthritis is unknown. We performed T<sub>H</sub>17 cell lineage tracing in the SKG mouse model of RA. In arthritic mice, synovial T<sub>H</sub>17 cells transdifferentiate into CD44<sup>+</sup> exT<sub>H</sub>17 cells, which are more arthritogenic and sustain inflammation that is IL-17 independent. The exT<sub>H</sub>17 cell gene signature includes up-regulation of CD44 and sphingosine-1-phosphate receptor 4 (S1PR4) and correlates with the profile of human RA synovial CD4<sup>+</sup> T cells. We demonstrate that cross-talk between T<sub>H</sub>17 cells and fibroblast-like synoviocytes (FLSs) via S1P promotes T<sub>H</sub>17-exT<sub>H</sub>17 cell conversion. CD44 is necessary for exT<sub>H</sub>17 cell–mediated arthritis. Our study suggests that FLS expansion during RA progression promotes T<sub>H</sub>17-exT<sub>H</sub>17 cell conversion. These results could potentially enable RA precision therapy.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 113","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145455363","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}
引用次数: 0
Stem-like tissue-resident memory T cells control functional heterogeneity and reactivation of T cell memory in the intestine 干细胞样组织驻留记忆T细胞控制肠中T细胞记忆的功能异质性和再激活
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-10-31 DOI: 10.1126/sciimmunol.adw1992
Kevin Man, Vinicius A. Duarte da Silva, Nikita Potemkin, Sarah S. Gabriel, Teisha Mason, Tarek Elmzzahi, Marcela De Lima Moreira, Chun-Hsi Su, Laura Mackay, Marc D. Beyer, Jan Schröder, Georg Gasteiger, Axel Kallies
Tissue-resident memory T (TRM) cells provide localized immunity against intracellular pathogens and cancer. Upon antigen reencounter, TRM cells differentiate into effector cells while also giving rise to another generation of memory cells. Here, we show that intestinal TRM cells that express the transcriptional regulators TCF1 or ID3 exhibit stem-like memory properties and are endowed with a superior capacity to regenerate effector and memory T cells after pathogen reencounter. Ablation of TCF1 using a TRM cell–specific mouse model resulted in impaired formation of intestinal TRM cells, altered their transcriptional heterogeneity, and increased their differentiation into tissue-confined and recirculating CX3CR1+ effector cells during recall. TGF-β and retinoic acid were required for formation and survival of TCF1- and ID3-expressing TRM cells and restrained their differentiation into CX3CR1+ effector cells during reinfection. Thus, stem-like cells control the quality and recall capacity of TRM cells, thereby contributing to anamnestic memory responses.
组织常驻记忆T (trm)细胞提供针对细胞内病原体和癌症的局部免疫。当再次遇到抗原时,T - RM细胞分化为效应细胞,同时也产生另一代记忆细胞。在这里,我们发现表达转录调控因子TCF1或ID3的肠T RM细胞表现出干细胞样记忆特性,并且在再次遇到病原体后具有再生效应T细胞和记忆T细胞的优越能力。使用T RM细胞特异性小鼠模型消融TCF1导致肠道T RM细胞形成受损,改变其转录异质性,并在回忆过程中增加其向组织受限和循环的CX3CR1 +效应细胞的分化。TGF-β和维甲酸是表达TCF1-和id3的T RM细胞形成和存活所必需的,并在再感染过程中抑制其向CX3CR1 +效应细胞的分化。因此,干细胞样细胞控制T - RM细胞的质量和回忆能力,从而促进遗忘记忆反应。
{"title":"Stem-like tissue-resident memory T cells control functional heterogeneity and reactivation of T cell memory in the intestine","authors":"Kevin Man,&nbsp;Vinicius A. Duarte da Silva,&nbsp;Nikita Potemkin,&nbsp;Sarah S. Gabriel,&nbsp;Teisha Mason,&nbsp;Tarek Elmzzahi,&nbsp;Marcela De Lima Moreira,&nbsp;Chun-Hsi Su,&nbsp;Laura Mackay,&nbsp;Marc D. Beyer,&nbsp;Jan Schröder,&nbsp;Georg Gasteiger,&nbsp;Axel Kallies","doi":"10.1126/sciimmunol.adw1992","DOIUrl":"10.1126/sciimmunol.adw1992","url":null,"abstract":"<div >Tissue-resident memory T (T<sub>RM</sub>) cells provide localized immunity against intracellular pathogens and cancer. Upon antigen reencounter, T<sub>RM</sub> cells differentiate into effector cells while also giving rise to another generation of memory cells. Here, we show that intestinal T<sub>RM</sub> cells that express the transcriptional regulators TCF1 or ID3 exhibit stem-like memory properties and are endowed with a superior capacity to regenerate effector and memory T cells after pathogen reencounter. Ablation of TCF1 using a T<sub>RM</sub> cell–specific mouse model resulted in impaired formation of intestinal T<sub>RM</sub> cells, altered their transcriptional heterogeneity, and increased their differentiation into tissue-confined and recirculating CX3CR1<sup>+</sup> effector cells during recall. TGF-β and retinoic acid were required for formation and survival of TCF1- and ID3-expressing T<sub>RM</sub> cells and restrained their differentiation into CX3CR1<sup>+</sup> effector cells during reinfection. Thus, stem-like cells control the quality and recall capacity of T<sub>RM</sub> cells, thereby contributing to anamnestic memory responses.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 112","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145405217","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}
引用次数: 0
RNA binding proteins control the G2-M checkpoint of the germinal center B cell RNA结合蛋白控制生发中心B细胞的g2 -M检查点
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-10-31 DOI: 10.1126/sciimmunol.adu3718
Fiamma Salerno, Alex J. Whale, Louise S. Matheson, Davide Vespasiani, William S. Foster, Twm J. Mitchell, Michael Screen, Melanie Stammers, Sarah E. Bell, Daniel J. Hodson, Hamish W. King, Michelle A. Linterman, Jonathan Houseley, Martin Turner
The germinal center (GC) reaction drives the production of high-affinity antibodies by iterative cycles of B cell somatic hypermutation, selection, and proliferation. How GC B cells undergo rapid cell division while maintaining genome stability is poorly understood. Here, we show that the RNA binding proteins ZFP36L1 and ZFP36L2 act downstream of antigen sensing and protect GC B cells from replication stress by controlling a cell cycle–related posttranscriptional regulon. They safeguard the successful completion of mitosis by balancing CDK1 and p21-mediated regulation of cell-cycle progression. In their absence, GC B cells are prone to arrest in the G2-M phase and die by apoptosis, resulting in curtailed GC responses. DNA replication forks stalled at active replication initiation zones, causing replication stress and increased activity of the ATR-CHK1 DNA damage response. Thus, RNA binding proteins guide posttranscriptional gene regulation and maintain a functional G2-M checkpoint in GC B cells.
生发中心(GC)反应通过B细胞体细胞超突变、选择和增殖的迭代循环驱动高亲和力抗体的产生。GC B细胞如何在保持基因组稳定性的同时进行快速细胞分裂尚不清楚。在这里,我们发现RNA结合蛋白ZFP36L1和ZFP36L2作用于抗原感应的下游,并通过控制细胞周期相关的转录后调控来保护GC B细胞免受复制应激。它们通过平衡CDK1和p21介导的细胞周期进程调节来保障有丝分裂的成功完成。在缺乏它们的情况下,GC B细胞容易在g2 -M期停滞并凋亡,导致GC反应减弱。DNA复制叉在主动复制起始区停滞,导致复制应激和ATR-CHK1 DNA损伤反应活性增加。因此,RNA结合蛋白在GC B细胞中引导转录后基因调控并维持功能的g2 -M检查点。
{"title":"RNA binding proteins control the G2-M checkpoint of the germinal center B cell","authors":"Fiamma Salerno,&nbsp;Alex J. Whale,&nbsp;Louise S. Matheson,&nbsp;Davide Vespasiani,&nbsp;William S. Foster,&nbsp;Twm J. Mitchell,&nbsp;Michael Screen,&nbsp;Melanie Stammers,&nbsp;Sarah E. Bell,&nbsp;Daniel J. Hodson,&nbsp;Hamish W. King,&nbsp;Michelle A. Linterman,&nbsp;Jonathan Houseley,&nbsp;Martin Turner","doi":"10.1126/sciimmunol.adu3718","DOIUrl":"10.1126/sciimmunol.adu3718","url":null,"abstract":"<div >The germinal center (GC) reaction drives the production of high-affinity antibodies by iterative cycles of B cell somatic hypermutation, selection, and proliferation. How GC B cells undergo rapid cell division while maintaining genome stability is poorly understood. Here, we show that the RNA binding proteins ZFP36L1 and ZFP36L2 act downstream of antigen sensing and protect GC B cells from replication stress by controlling a cell cycle–related posttranscriptional regulon. They safeguard the successful completion of mitosis by balancing CDK1 and p21-mediated regulation of cell-cycle progression. In their absence, GC B cells are prone to arrest in the G<sub>2</sub>-M phase and die by apoptosis, resulting in curtailed GC responses. DNA replication forks stalled at active replication initiation zones, causing replication stress and increased activity of the ATR-CHK1 DNA damage response. Thus, RNA binding proteins guide posttranscriptional gene regulation and maintain a functional G<sub>2</sub>-M checkpoint in GC B cells.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 112","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145405215","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}
引用次数: 0
Local activation of mutant RIG-I by short noncoding Y-RNA in the kidney triggers lethal nephritis 肾脏中短的非编码Y-RNA局部激活突变RIG-I可引发致死性肾炎
IF 16.3 1区 医学 Q1 IMMUNOLOGY Pub Date : 2025-10-31 DOI: 10.1126/sciimmunol.adx1135
Saya Satoh, Yaw Bia Tan, Benjamin Heil, Shintaro Yamada, Verena Schütte, Celest Phang, Chaozhi Tang, Yuta Tsukamoto, Takahiro Higuchi, Takashi Fujita, Rayk Behrendt, Martin Schlee, Dahai Luo, Hiroki Kato
Detecting viral RNA by the ubiquitously expressed cytosolic receptor retinoic acid–inducible gene I (RIG-I) is critical for antiviral immune responses, including type I interferon (IFN-I) and chemokine induction. RIG-I has evolved to sensitively recognize viral RNA but tolerate self-RNA. RIG-I mutations causing self-tolerance loss induce IFN-I and chemokines in patients, initiating autoinflammation. We observed that mice expressing the RIG-I patient variant E373A spontaneously developed lupus-like nephritis. Kidney-derived chemokines attracted monocytes through CCR2 (C-C motif chemokine receptor 2) and induced interstitial inflammation and tubular damage. This led to renal dysfunction independently of immunoglobulin G–nucleic acid complex deposition. Sequencing of RIG-I E373A–bound RNA from kidney-derived cells identified short noncoding Y-RNA. Deletion of the most enriched Y-RNA species reduced RIG-I E373A–induced IFN-I responses. Cryo–electron microscopy and molecular analyses revealed that RIG-I E373A binding to the Y-RNA stem region resulted in its activation. Thus, we demonstrate that Y-RNA activates a RIG-I gain-of-function mutant in a tissue-specific manner, causing autoinflammation culminating in lupus nephritis.
通过普遍表达的胞质受体维甲酸诱导基因I (RIG-I)检测病毒RNA对抗病毒免疫反应至关重要,包括I型干扰素(IFN-I)和趋化因子诱导。rig - 1已经进化到敏感地识别病毒RNA,但耐受自身RNA。RIG-I突变导致患者自身耐受性丧失,诱导IFN-I和趋化因子,引发自身炎症。我们观察到,表达RIG-I患者变体E373A的小鼠自发发展为狼疮样肾炎。肾源性趋化因子通过CCR2 (C-C基序趋化因子受体2)吸引单核细胞,诱导间质炎症和肾小管损伤。这导致肾功能障碍独立于免疫球蛋白g -核酸复合物沉积。肾源性细胞RIG-I e373a结合RNA测序鉴定出短的非编码Y-RNA。删除最富集的Y-RNA物种可降低RIG-I e373a诱导的IFN-I反应。冷冻电镜和分子分析显示RIG-I E373A与Y-RNA干区结合导致其活化。因此,我们证明Y-RNA以组织特异性的方式激活RIG-I功能获得突变,导致自身炎症最终导致狼疮性肾炎。
{"title":"Local activation of mutant RIG-I by short noncoding Y-RNA in the kidney triggers lethal nephritis","authors":"Saya Satoh,&nbsp;Yaw Bia Tan,&nbsp;Benjamin Heil,&nbsp;Shintaro Yamada,&nbsp;Verena Schütte,&nbsp;Celest Phang,&nbsp;Chaozhi Tang,&nbsp;Yuta Tsukamoto,&nbsp;Takahiro Higuchi,&nbsp;Takashi Fujita,&nbsp;Rayk Behrendt,&nbsp;Martin Schlee,&nbsp;Dahai Luo,&nbsp;Hiroki Kato","doi":"10.1126/sciimmunol.adx1135","DOIUrl":"10.1126/sciimmunol.adx1135","url":null,"abstract":"<div >Detecting viral RNA by the ubiquitously expressed cytosolic receptor retinoic acid–inducible gene I (RIG-I) is critical for antiviral immune responses, including type I interferon (IFN-I) and chemokine induction. RIG-I has evolved to sensitively recognize viral RNA but tolerate self-RNA. RIG-I mutations causing self-tolerance loss induce IFN-I and chemokines in patients, initiating autoinflammation. We observed that mice expressing the RIG-I patient variant E373A spontaneously developed lupus-like nephritis. Kidney-derived chemokines attracted monocytes through CCR2 (C-C motif chemokine receptor 2) and induced interstitial inflammation and tubular damage. This led to renal dysfunction independently of immunoglobulin G–nucleic acid complex deposition. Sequencing of RIG-I E373A–bound RNA from kidney-derived cells identified short noncoding Y-RNA. Deletion of the most enriched Y-RNA species reduced RIG-I E373A–induced IFN-I responses. Cryo–electron microscopy and molecular analyses revealed that RIG-I E373A binding to the Y-RNA stem region resulted in its activation. Thus, we demonstrate that Y-RNA activates a RIG-I gain-of-function mutant in a tissue-specific manner, causing autoinflammation culminating in lupus nephritis.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 112","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145405216","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}
引用次数: 0
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Science Immunology
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