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Erratum for the Research Article “TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf” by Y. Chang et al. Y. Chang 等人的研究文章 "TGF-β 通过 c-Maf 指定小鼠 CD4+ T 细胞中 TFH 与 TH17 细胞的命运 "的勘误。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-09 DOI: 10.1126/sciimmunol.adr7181
{"title":"Erratum for the Research Article “TGF-β specifies TFH versus TH17 cell fates in murine CD4+ T cells through c-Maf” by Y. Chang et al.","authors":"","doi":"10.1126/sciimmunol.adr7181","DOIUrl":"10.1126/sciimmunol.adr7181","url":null,"abstract":"","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141910109","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
SARS-CoV-2 JN.1 variant evasion of IGHV3-53/3-66 B cell germlines SARS-CoV-2 JN.1 变体对 IGHV3-53/3-66 B 细胞种系的规避。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-09 DOI: 10.1126/sciimmunol.adp9279
Ida Paciello, Giuseppe Maccari, Giulio Pierleoni, Federica Perrone, Giulia Realini, Marco Troisi, Gabriele Anichini, Maria Grazia Cusi, Rino Rappuoli, Emanuele Andreano
{"title":"SARS-CoV-2 JN.1 variant evasion of IGHV3-53/3-66 B cell germlines","authors":"Ida Paciello,&nbsp;Giuseppe Maccari,&nbsp;Giulio Pierleoni,&nbsp;Federica Perrone,&nbsp;Giulia Realini,&nbsp;Marco Troisi,&nbsp;Gabriele Anichini,&nbsp;Maria Grazia Cusi,&nbsp;Rino Rappuoli,&nbsp;Emanuele Andreano","doi":"10.1126/sciimmunol.adp9279","DOIUrl":"10.1126/sciimmunol.adp9279","url":null,"abstract":"<div >The severe acute respiratory syndrome coronavirus 2 variant JN.1 recently emerged as the dominant variant despite having only one amino acid change on the spike (S) protein receptor binding domain (RBD) compared with the ancestral BA.2.86, which never represented more than 5% of global variants. To define at the molecular level the JN.1 ability to spread globally, we interrogated a panel of 899 neutralizing human monoclonal antibodies. Our data show that the single leucine-455–to–serine mutation in the JN.1 spike protein RBD unleashed the global spread of JN.1, likely occurring by elimination of more than 70% of the neutralizing antibodies mediated by IGHV3-53/3-66 germlines. However, the resilience of class 3 antibodies with low neutralization potency but strong Fc functions may explain the absence of JN.1 severe disease.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adp9279","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141910110","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}
引用次数: 0
B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting 当抗原具有局限性时,B 细胞需要 DOCK8 来激发和整合 T 细胞的帮助。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-09 DOI: 10.1126/sciimmunol.add4874
Mukta Deobagkar-Lele, Greg Crawford, Tanya L. Crockford, Jennifer Back, Rose Hodgson, Aneesha Bhandari, Katherine R. Bull, Richard J. Cornall
{"title":"B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting","authors":"Mukta Deobagkar-Lele,&nbsp;Greg Crawford,&nbsp;Tanya L. Crockford,&nbsp;Jennifer Back,&nbsp;Rose Hodgson,&nbsp;Aneesha Bhandari,&nbsp;Katherine R. Bull,&nbsp;Richard J. Cornall","doi":"10.1126/sciimmunol.add4874","DOIUrl":"10.1126/sciimmunol.add4874","url":null,"abstract":"<div >Dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome is characterized by a failure of the germinal center response, a process involving the proliferation and positive selection of antigen-specific B cells. Here, we describe how DOCK8-deficient B cells are blocked at a light-zone checkpoint in the germinal centers of immunized mice, where they are unable to respond to T cell–dependent survival and selection signals and consequently differentiate into plasma cells or memory B cells. Although DOCK8-deficient B cells can acquire and present antigen to initiate activation of cognate T cells, integrin up-regulation, B cell–T cell conjugate formation, and costimulation are insufficient for sustained B cell and T cell activation when antigen availability is limited. Our findings provide an explanation for the failure of the humoral response in DOCK8 immunodeficiency syndrome and insight into how the level of available antigen modulates B cell–T cell cross-talk to fine-tune humoral immune responses and immunological memory.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141910108","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
The human CD47 checkpoint is targeted by an immunosuppressive Aedes aegypti salivary factor to enhance arboviral skin infectivity 埃及伊蚊唾液免疫抑制因子以人类 CD47 检查点为靶点,增强了虫媒病毒的皮肤传染性。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-09 DOI: 10.1126/sciimmunol.adk9872
Alejandro Marin-Lopez, John D. Huck, Allen T. Esterly, Veronica Azcutia, Connor Rosen, Rolando Garcia-Milian, Esen Sefik, Gemma Vidal-Pedrola, Hamidah Raduwan, Tse-Yu Chen, Gunjan Arora, Stephanie Halene, Albert C. Shaw, Noah W. Palm, Richard A. Flavell, Charles A. Parkos, Saravanan Thangamani, Aaron M. Ring, Erol Fikrig
{"title":"The human CD47 checkpoint is targeted by an immunosuppressive Aedes aegypti salivary factor to enhance arboviral skin infectivity","authors":"Alejandro Marin-Lopez,&nbsp;John D. Huck,&nbsp;Allen T. Esterly,&nbsp;Veronica Azcutia,&nbsp;Connor Rosen,&nbsp;Rolando Garcia-Milian,&nbsp;Esen Sefik,&nbsp;Gemma Vidal-Pedrola,&nbsp;Hamidah Raduwan,&nbsp;Tse-Yu Chen,&nbsp;Gunjan Arora,&nbsp;Stephanie Halene,&nbsp;Albert C. Shaw,&nbsp;Noah W. Palm,&nbsp;Richard A. Flavell,&nbsp;Charles A. Parkos,&nbsp;Saravanan Thangamani,&nbsp;Aaron M. Ring,&nbsp;Erol Fikrig","doi":"10.1126/sciimmunol.adk9872","DOIUrl":"10.1126/sciimmunol.adk9872","url":null,"abstract":"<div >The <i>Aedes aegypti</i> mosquito is a vector of many infectious agents, including flaviviruses such as Zika virus. Components of mosquito saliva have pleomorphic effects on the vertebrate host to enhance blood feeding, and these changes also create a favorable niche for pathogen replication and dissemination. Here, we demonstrate that human CD47, which is known to be involved in various immune processes, interacts with a 34-kilodalton mosquito salivary protein named Nest1. Nest1 is up-regulated in blood-fed female <i>A. aegypti</i> and facilitates Zika virus dissemination in human skin explants. Nest1 has a stronger affinity for CD47 than its natural ligand, signal regulatory protein α, competing for binding at the same interface. The interaction between Nest1 with CD47 suppresses phagocytosis by human macrophages and inhibits proinflammatory responses by white blood cells, thereby suppressing antiviral responses in the skin. This interaction elucidates how an arthropod protein alters the human response to promote arbovirus infectivity.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141910111","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
cGAS-activated endothelial cell–T cell cross-talk initiates tertiary lymphoid structure formation cGAS 激活的内皮细胞-T 细胞交叉对话启动了三级淋巴结构的形成。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-02 DOI: 10.1126/sciimmunol.adk2612
Ruibo Zhao, Jinghe Zhang, Jialu Ma, Yali Qu, Zhenrong Yang, Zhinan Yin, Fengyin Li, Zhongjun Dong, Qinmiao Sun, Shu Zhu, Zhijian J. Chen, Daxing Gao
{"title":"cGAS-activated endothelial cell–T cell cross-talk initiates tertiary lymphoid structure formation","authors":"Ruibo Zhao,&nbsp;Jinghe Zhang,&nbsp;Jialu Ma,&nbsp;Yali Qu,&nbsp;Zhenrong Yang,&nbsp;Zhinan Yin,&nbsp;Fengyin Li,&nbsp;Zhongjun Dong,&nbsp;Qinmiao Sun,&nbsp;Shu Zhu,&nbsp;Zhijian J. Chen,&nbsp;Daxing Gao","doi":"10.1126/sciimmunol.adk2612","DOIUrl":"10.1126/sciimmunol.adk2612","url":null,"abstract":"<div >Aberrant activation of the cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes (cGAS-STING) pathway causes autoimmunity in humans and mice; however, the exact mechanism by which the cGAS-STING pathway initiates adaptive immunity and tissue pathology is still not fully understood. Here, we used a cGAS knockin (KI) mouse model that develops systemic autoimmunity. In the lungs of cGAS-KI mice, blood vessels were enclosed by organized lymphoid tissues that resemble tertiary lymphoid structures (TLSs). Cell-intrinsic cGAS induction promoted up-regulation of CCR5 in CD8<sup>+</sup> T cells and led to CCL5 production in vascular endothelial cells. Peripheral CD8<sup>+</sup> T cells were recruited to the lungs and produced CXCL13 and interferon-γ. The latter triggered endothelial cell death, potentiated CCL5 production, and was essential for TLS establishment. Blocking CCL5 or CCR5, or depleting CD8<sup>+</sup> T cells, impaired TLS formation. cGAS-mediated TLS formation also enhanced humoral and antitumor responses. These data demonstrate that cGAS signaling drives a specialized lymphoid structure that underlies autoimmune tissue pathology.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adk2612","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879343","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}
引用次数: 0
Recruited atypical Ly6G+ macrophages license alveolar regeneration after lung injury 肺损伤后招募的非典型 Ly6G+ 巨噬细胞许可肺泡再生
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-02 DOI: 10.1126/sciimmunol.ado1227
Cecilia Ruscitti, Joan Abinet, Pauline Maréchal, Margot Meunier, Constance de Meeûs, Domien Vanneste, Pierre Janssen, Mickael Dourcy, Marc Thiry, Fabrice Bureau, Christoph Schneider, Benedicte Machiels, Andres Hidalgo, Florent Ginhoux, Benjamin G. Dewals, Julien Guiot, Florence Schleich, Mutien-Marie Garigliany, Akeila Bellahcène, Coraline Radermecker, Thomas Marichal
{"title":"Recruited atypical Ly6G+ macrophages license alveolar regeneration after lung injury","authors":"Cecilia Ruscitti,&nbsp;Joan Abinet,&nbsp;Pauline Maréchal,&nbsp;Margot Meunier,&nbsp;Constance de Meeûs,&nbsp;Domien Vanneste,&nbsp;Pierre Janssen,&nbsp;Mickael Dourcy,&nbsp;Marc Thiry,&nbsp;Fabrice Bureau,&nbsp;Christoph Schneider,&nbsp;Benedicte Machiels,&nbsp;Andres Hidalgo,&nbsp;Florent Ginhoux,&nbsp;Benjamin G. Dewals,&nbsp;Julien Guiot,&nbsp;Florence Schleich,&nbsp;Mutien-Marie Garigliany,&nbsp;Akeila Bellahcène,&nbsp;Coraline Radermecker,&nbsp;Thomas Marichal","doi":"10.1126/sciimmunol.ado1227","DOIUrl":"10.1126/sciimmunol.ado1227","url":null,"abstract":"<div >The lung is constantly exposed to airborne pathogens and particles that can cause alveolar damage. Hence, appropriate repair responses are essential for gas exchange and life. Here, we deciphered the spatiotemporal trajectory and function of an atypical population of macrophages after lung injury. Post–influenza A virus (IAV) infection, short-lived monocyte-derived Ly6G-expressing macrophages (Ly6G<sup>+</sup> Macs) were recruited to the alveoli of lung perilesional areas. Ly6G<sup>+</sup> Macs engulfed immune cells, exhibited a high metabolic potential, and clustered with alveolar type 2 epithelial cells (AT2s) in zones of active epithelial regeneration. Ly6G<sup>+</sup> Macs were partially dependent on granulocyte-macrophage colony-stimulating factor and interleukin-4 receptor signaling and were essential for AT2-dependent alveolar regeneration. Similar macrophages were recruited in other models of injury and in the airspaces of lungs from patients with suspected pneumonia. This study identifies perilesional alveolar Ly6G<sup>+</sup> Macs as a spatially restricted, short-lived macrophage subset promoting epithelial regeneration postinjury, thus representing an attractive therapeutic target for treating lung damage.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879346","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
Enough already: T cell inflammation and SARS-CoV-2 virus persist in Long Covid 已经够了T 细胞炎症和 SARS-CoV-2 病毒在 Long Covid 持续存在。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-02 DOI: 10.1126/sciimmunol.adr9661
Rachael A. Clark
{"title":"Enough already: T cell inflammation and SARS-CoV-2 virus persist in Long Covid","authors":"Rachael A. Clark","doi":"10.1126/sciimmunol.adr9661","DOIUrl":"10.1126/sciimmunol.adr9661","url":null,"abstract":"<div >Virus and T cell inflammation persist in the tissues of patients with Long Covid.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879344","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
The yeast also rises! PD-L1 dampens inflammation linked to fungal infections 酵母菌也会上升!PD-L1 可抑制与真菌感染有关的炎症。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-02 DOI: 10.1126/sciimmunol.adr9663
Sultan AlSalem, Shiv Pillai
{"title":"The yeast also rises! PD-L1 dampens inflammation linked to fungal infections","authors":"Sultan AlSalem,&nbsp;Shiv Pillai","doi":"10.1126/sciimmunol.adr9663","DOIUrl":"10.1126/sciimmunol.adr9663","url":null,"abstract":"<div >Programmed death-ligand 1 interacts with fungal ribosomal Rpl20b in phagosomes and induces interleukin-10 secretion.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879347","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
Never trust a single myeloid marker: Ly6G on repair-promoting lung macrophages 永远不要相信单一的骨髓标志物促进修复的肺巨噬细胞上的 Ly6G。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-08-02 DOI: 10.1126/sciimmunol.adq7306
Chrysante S. Iliakis, Andreas Wack
{"title":"Never trust a single myeloid marker: Ly6G on repair-promoting lung macrophages","authors":"Chrysante S. Iliakis,&nbsp;Andreas Wack","doi":"10.1126/sciimmunol.adq7306","DOIUrl":"10.1126/sciimmunol.adq7306","url":null,"abstract":"<div >Short-lived repair-promoting macrophages are recruited to foci of lung damage during influenza infection—and they are Ly6G positive (see related Research Article by Ruscitti <i>et al.</i>).</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 98","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879345","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
Sterile production of interferons in the thymus affects T cell repertoire selection 胸腺中干扰素的无菌产生会影响 T 细胞的选择。
IF 17.6 1区 医学
Science Immunology Pub Date : 2024-07-26 DOI: 10.1126/sciimmunol.adp1139
K. Maude Ashby, Matouš Vobořil, Oscar C. Salgado, S. Thera Lee, Ryan J. Martinez, Christine H. O’Connor, Elise R. Breed, Shuya Xuan, Charles R. Roll, Saumith Bachigari, Hattie Heiland, Daniel B. Stetson, Sergei V. Kotenko, Kristin A. Hogquist
{"title":"Sterile production of interferons in the thymus affects T cell repertoire selection","authors":"K. Maude Ashby,&nbsp;Matouš Vobořil,&nbsp;Oscar C. Salgado,&nbsp;S. Thera Lee,&nbsp;Ryan J. Martinez,&nbsp;Christine H. O’Connor,&nbsp;Elise R. Breed,&nbsp;Shuya Xuan,&nbsp;Charles R. Roll,&nbsp;Saumith Bachigari,&nbsp;Hattie Heiland,&nbsp;Daniel B. Stetson,&nbsp;Sergei V. Kotenko,&nbsp;Kristin A. Hogquist","doi":"10.1126/sciimmunol.adp1139","DOIUrl":"10.1126/sciimmunol.adp1139","url":null,"abstract":"<div >Type I and III interferons (IFNs) are robustly induced during infections and protect cells against viral infection. Both type I and III IFNs are also produced at low levels in the thymus at steady state; however, their role in T cell development and immune tolerance is unclear. Here, we found that both type I and III IFNs were constitutively produced by a very small number of AIRE<sup>+</sup> murine thymic epithelial cells, independent of microbial stimulation. Antigen-presenting cells were highly responsive to thymic IFNs, and IFNs were required for the activation and maturation of thymic type 1 conventional dendritic cells, macrophages, and B cells. Loss of IFN sensing led to reduced regulatory T cell selection, reduced T cell receptor (TCR) repertoire diversity, and enhanced autoreactive T cell responses to self-antigens expressed during peripheral IFN signaling. Thus, constitutive exposure to IFNs in the thymus is required for generating a tolerant and diverse TCR repertoire.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 97","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141767306","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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