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The role of interleukin-17 in tumor development and progression 白细胞介素-17在肿瘤发生发展中的作用
Pub Date : 2019-11-14 DOI: 10.1084/jem.20190297
Junjie Zhao, Xing Chen, T. Herjan, Xiaoxia Li
This review discusses the growing literature on the pathogenic role of IL-17 in cancer, focusing on recent studies that place IL-17 as a nexus linking inflammation, tissue repair, and cancer.
本文讨论了越来越多的关于IL-17在癌症中的致病作用的文献,重点介绍了IL-17在炎症、组织修复和癌症之间的联系。
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引用次数: 116
B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2 B细胞对乳糜泻自身抗原转谷氨酰胺酶2的耐受性和抗体产生
Pub Date : 2019-11-14 DOI: 10.1084/jem.20190860
M. F. du Pre, Jana Blaževski, Alisa E. Dewan, J. Stamnaes, Chakravarthi Kanduri, G. K. Sandve, M. K. Johannesen, Christian B Lindstad, Kathrin Hnida, L. Fugger, G. Melino, Shuo-Wang Qiao, L. Sollid
This study sheds light on the mechanism by which autoantibodies to transglutaminase 2 (TG2) are formed in celiac disease. The authors find that there is no deletion or silencing of autoreactive TG2-specific B cells and that production of anti-TG2 autoantibodies is controlled by T cell help.
本研究揭示了在乳糜泻中形成转谷氨酰胺酶2 (TG2)自身抗体的机制。作者发现自身反应性tg2特异性B细胞没有缺失或沉默,抗tg2自身抗体的产生是由T细胞帮助控制的。
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引用次数: 37
Targeting the interleukin-17 immune axis for cancer immunotherapy 靶向白细胞介素-17免疫轴的癌症免疫治疗
Pub Date : 2019-11-14 DOI: 10.1084/jem.20190456
G. Vitiello, G. Miller
IL-17 plays versatile roles during tumorigenesis. Here, Vitiello and Miller summarize current knowledge in harnessing IL-17–producing γδ and Th17 cells for successful cancer immunotherapy.
IL-17在肿瘤发生过程中发挥多种作用。在这里,Vitiello和Miller总结了利用产生il -17的γδ和Th17细胞成功进行癌症免疫治疗的现有知识。
{"title":"Targeting the interleukin-17 immune axis for cancer immunotherapy","authors":"G. Vitiello, G. Miller","doi":"10.1084/jem.20190456","DOIUrl":"https://doi.org/10.1084/jem.20190456","url":null,"abstract":"IL-17 plays versatile roles during tumorigenesis. Here, Vitiello and Miller summarize current knowledge in harnessing IL-17–producing γδ and Th17 cells for successful cancer immunotherapy.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74064434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 82
Interleukin-17 cytokines: Effectors and targets in psoriasis—A breakthrough in understanding and treatment 白介素-17细胞因子:银屑病的效应因子和靶点——认识和治疗的突破
Pub Date : 2019-11-14 DOI: 10.1084/jem.20191397
I. Prinz, I. Sandrock, U. Mrowietz
This review summarizes the steps from basic research on IL-17 family cytokines to understanding their role in psoriasis pathogenesis to the approval of a number of monoclonal antibodies targeting IL-17 pathways as first line treatment of psoriasis and psoriatic arthritis.
本文综述了从IL-17家族细胞因子的基础研究到了解其在银屑病发病机制中的作用,再到一些靶向IL-17通路的单克隆抗体被批准作为银屑病和银屑病关节炎的一线治疗方法。
{"title":"Interleukin-17 cytokines: Effectors and targets in psoriasis—A breakthrough in understanding and treatment","authors":"I. Prinz, I. Sandrock, U. Mrowietz","doi":"10.1084/jem.20191397","DOIUrl":"https://doi.org/10.1084/jem.20191397","url":null,"abstract":"This review summarizes the steps from basic research on IL-17 family cytokines to understanding their role in psoriasis pathogenesis to the approval of a number of monoclonal antibodies targeting IL-17 pathways as first line treatment of psoriasis and psoriatic arthritis.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81608228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 47
Targeting interleukin-17 in chronic inflammatory disease: A clinical perspective 靶向白介素-17治疗慢性炎性疾病的临床研究
Pub Date : 2019-11-14 DOI: 10.1084/jem.20191123
P. Zwicky, S. Unger, B. Becher
Although many chronic inflammatory diseases share the feature of elevated IL-17 production, therapeutic targeting of IL-17 has vastly different clinical outcomes. Here the authors summarize the recent progress in understanding the protective and pathogenic role of the IL-23/IL-17 axis in preclinical models and human inflammatory diseases.
尽管许多慢性炎症性疾病都具有IL-17产生升高的特征,但IL-17的靶向治疗具有截然不同的临床结果。本文综述了IL-23/IL-17轴在临床前模型和人类炎症性疾病中的保护和致病作用的最新进展。
{"title":"Targeting interleukin-17 in chronic inflammatory disease: A clinical perspective","authors":"P. Zwicky, S. Unger, B. Becher","doi":"10.1084/jem.20191123","DOIUrl":"https://doi.org/10.1084/jem.20191123","url":null,"abstract":"Although many chronic inflammatory diseases share the feature of elevated IL-17 production, therapeutic targeting of IL-17 has vastly different clinical outcomes. Here the authors summarize the recent progress in understanding the protective and pathogenic role of the IL-23/IL-17 axis in preclinical models and human inflammatory diseases.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86986746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 59
Mevalonate metabolism–dependent protein geranylgeranylation regulates thymocyte egress 甲羟戊酸代谢依赖蛋白香叶酰化调节胸腺细胞的分泌
Pub Date : 2019-11-13 DOI: 10.1084/jem.20190969
Xingrong Du, H. Zeng, Shaofeng Liu, C. Guy, Yogesh Dhungana, G. Neale, M. Bergo, H. Chi
Thymocyte egress is a critical determinant of T cell homeostasis and adaptive immunity. Du et al. describe unexpected roles of mevalonate metabolism–fueled protein geranylgeranylation, but not farnesylation, in driving thymocyte egress through modulating Cdc42 and Pak activities.
胸腺细胞的输出是T细胞稳态和适应性免疫的关键决定因素。Du等人描述了甲羟戊酸代谢驱动的蛋白香叶酰化(而非法酰化)在通过调节Cdc42和Pak活性驱动胸腺细胞输出中的意想不到的作用。
{"title":"Mevalonate metabolism–dependent protein geranylgeranylation regulates thymocyte egress","authors":"Xingrong Du, H. Zeng, Shaofeng Liu, C. Guy, Yogesh Dhungana, G. Neale, M. Bergo, H. Chi","doi":"10.1084/jem.20190969","DOIUrl":"https://doi.org/10.1084/jem.20190969","url":null,"abstract":"Thymocyte egress is a critical determinant of T cell homeostasis and adaptive immunity. Du et al. describe unexpected roles of mevalonate metabolism–fueled protein geranylgeranylation, but not farnesylation, in driving thymocyte egress through modulating Cdc42 and Pak activities.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87255288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
Tyrosine kinase inhibitor imatinib augments tumor immunity by depleting effector regulatory T cells 酪氨酸激酶抑制剂伊马替尼通过消耗效应调节性T细胞增强肿瘤免疫
Pub Date : 2019-11-08 DOI: 10.1084/jem.20191009
A. Tanaka, H. Nishikawa, Shinsuke Noguchi, D. Sugiyama, Hiromasa Morikawa, Yoshiko Takeuchi, D. Ha, Naoya Shigeta, T. Kitawaki, Y. Maeda, Takuro Saito, Yoshinori Shinohara, Y. Kameoka, K. Iwaisako, F. Monma, K. Ohishi, J. Karbach, E. Jäger, K. Sawada, N. Katayama, N. Takahashi, S. Sakaguchi
As a novel type of anticancer reagent, imatinib inhibits not only BCR-ABL oncogenic protein but also LCK in T cells as an off-target, being able to selectively deplete mature T reg cells and thereby evoke effective immune responses to various cancers.
作为一种新型的抗癌试剂,伊马替尼不仅可以抑制BCR-ABL致癌蛋白,还可以作为脱靶抑制T细胞中的LCK,能够选择性地消耗成熟T细胞,从而引起对各种癌症的有效免疫反应。
{"title":"Tyrosine kinase inhibitor imatinib augments tumor immunity by depleting effector regulatory T cells","authors":"A. Tanaka, H. Nishikawa, Shinsuke Noguchi, D. Sugiyama, Hiromasa Morikawa, Yoshiko Takeuchi, D. Ha, Naoya Shigeta, T. Kitawaki, Y. Maeda, Takuro Saito, Yoshinori Shinohara, Y. Kameoka, K. Iwaisako, F. Monma, K. Ohishi, J. Karbach, E. Jäger, K. Sawada, N. Katayama, N. Takahashi, S. Sakaguchi","doi":"10.1084/jem.20191009","DOIUrl":"https://doi.org/10.1084/jem.20191009","url":null,"abstract":"As a novel type of anticancer reagent, imatinib inhibits not only BCR-ABL oncogenic protein but also LCK in T cells as an off-target, being able to selectively deplete mature T reg cells and thereby evoke effective immune responses to various cancers.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79815893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 58
Glutamylation of deubiquitinase BAP1 controls self-renewal of hematopoietic stem cells and hematopoiesis 去泛素酶BAP1的谷氨酰化控制造血干细胞的自我更新和造血
Pub Date : 2019-11-07 DOI: 10.1084/jem.20190974
Zhen Xiong, P. Xia, Xiaoxiao Zhu, Jingjing Geng, Shuo Wang, B. Ye, Xiwen Qin, Yuan Qu, Luyun He, Dongdong Fan, Ying Du, Yong Tian, Z. Fan
Xiong et al. show that CCP3 performs deglutamylation of BAP1 to stabilize BAP1, which eliminates H2AK119Ub from Hoxa1 promoter and initiates Hoxa1 expression, leading to enhanced HSC self-renewal.
Xiong等人的研究表明,CCP3通过BAP1的去谷氨酰化来稳定BAP1,从而消除Hoxa1启动子中的H2AK119Ub,启动Hoxa1表达,从而增强HSC自我更新。
{"title":"Glutamylation of deubiquitinase BAP1 controls self-renewal of hematopoietic stem cells and hematopoiesis","authors":"Zhen Xiong, P. Xia, Xiaoxiao Zhu, Jingjing Geng, Shuo Wang, B. Ye, Xiwen Qin, Yuan Qu, Luyun He, Dongdong Fan, Ying Du, Yong Tian, Z. Fan","doi":"10.1084/jem.20190974","DOIUrl":"https://doi.org/10.1084/jem.20190974","url":null,"abstract":"Xiong et al. show that CCP3 performs deglutamylation of BAP1 to stabilize BAP1, which eliminates H2AK119Ub from Hoxa1 promoter and initiates Hoxa1 expression, leading to enhanced HSC self-renewal.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86640986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 8
ILC2s are the predominant source of intestinal ILC-derived IL-10 ILC2s是肠道IL-10来源的主要来源
Pub Date : 2019-11-07 DOI: 10.1084/jem.20191520
Jennifer K. Bando, S. Gilfillan, B. Di Luccia, J. L. Fachi, Cristiane Sécca, M. Cella, M. Colonna
This study shows that the regulatory innate lymphoid cell (ILCreg), a recently described IL-10–producing innate lymphocyte, is not present in mice bred in four different facilities. Instead, group 2 ILCs provide an inducible source of IL-10 in the intestine.
这项研究表明,在四种不同设施中饲养的小鼠中不存在调节性先天淋巴细胞(ILCreg),这是一种最近被描述的产生il -10的先天淋巴细胞。相反,2组IL-10在肠道中提供了诱导源。
{"title":"ILC2s are the predominant source of intestinal ILC-derived IL-10","authors":"Jennifer K. Bando, S. Gilfillan, B. Di Luccia, J. L. Fachi, Cristiane Sécca, M. Cella, M. Colonna","doi":"10.1084/jem.20191520","DOIUrl":"https://doi.org/10.1084/jem.20191520","url":null,"abstract":"This study shows that the regulatory innate lymphoid cell (ILCreg), a recently described IL-10–producing innate lymphocyte, is not present in mice bred in four different facilities. Instead, group 2 ILCs provide an inducible source of IL-10 in the intestine.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73830756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 78
Endothelial Cdk5 deficit leads to the development of spontaneous epilepsy through CXCL1/CXCR2-mediated reactive astrogliosis 内皮细胞Cdk5缺陷通过CXCL1/ cxcr2介导的反应性星形胶质细胞形成导致自发性癫痫的发生
Pub Date : 2019-11-07 DOI: 10.1084/jem.20180992
Xiuxiu Liu, Lin Yang, Ling-Xiao Shao, Yang He, Gang Wu, Y. Bao, Nan-nan Lu, Dong-Mei Gong, Yangyang Lu, Tian-Tian Cui, Ninghe Sun, Dan-yang Chen, W. Shi, K. Fukunaga, Hong-Shan Chen, Zhong Chen, Feng Han, Ying-Mei Lu
Liu et al. reveal a key mechanism that mediating the transition from cerebrovascular damage to epilepsy. They identify the endothelial cyclin-dependent kinase 5 (CDK5) regulates astrocytic glutamate reuptake and increased glutamate synaptic function through CXCL1/CXCR2-mediated astrogliosis.
Liu等人揭示了脑血管损伤向癫痫转变的关键机制。他们发现内皮细胞周期蛋白依赖性激酶5 (CDK5)通过CXCL1/ cxcr2介导的星形胶质细胞形成调节星形细胞谷氨酸再摄取和谷氨酸突触功能增加。
{"title":"Endothelial Cdk5 deficit leads to the development of spontaneous epilepsy through CXCL1/CXCR2-mediated reactive astrogliosis","authors":"Xiuxiu Liu, Lin Yang, Ling-Xiao Shao, Yang He, Gang Wu, Y. Bao, Nan-nan Lu, Dong-Mei Gong, Yangyang Lu, Tian-Tian Cui, Ninghe Sun, Dan-yang Chen, W. Shi, K. Fukunaga, Hong-Shan Chen, Zhong Chen, Feng Han, Ying-Mei Lu","doi":"10.1084/jem.20180992","DOIUrl":"https://doi.org/10.1084/jem.20180992","url":null,"abstract":"Liu et al. reveal a key mechanism that mediating the transition from cerebrovascular damage to epilepsy. They identify the endothelial cyclin-dependent kinase 5 (CDK5) regulates astrocytic glutamate reuptake and increased glutamate synaptic function through CXCL1/CXCR2-mediated astrogliosis.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78339048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 32
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The Tokushima journal of experimental medicine
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