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Histone methyltransferase Nsd2 is required for follicular helper T cell differentiation 组蛋白甲基转移酶Nsd2是滤泡辅助性T细胞分化所必需的
Pub Date : 2019-10-21 DOI: 10.1084/jem.20190832
Xuehui Long, Le Zhang, Yang Zhang, Min Min, Bichun Lin, Jingjing Chen, Xiaojie Ma, Sulan Zhai, Zhenming Cai, Yingxia Liu, Yanlai Lu, N. Che, W. Tan, J. Qin, Xiaoming Wang
Regulation of Bcl6 expression during follicular helper T cell differentiation remains incompletely understood. Here, Long et al. show that T cell activation induces H3K36me2 methyltransferase Nsd2, in a CD28- and ICOS-dependent manner, to promote Bcl6 expression and Tfh differentiation.
在滤泡辅助性T细胞分化过程中Bcl6表达的调控尚不完全清楚。在这里,Long等人发现T细胞激活诱导H3K36me2甲基转移酶Nsd2,以CD28和icos依赖的方式,促进Bcl6表达和Tfh分化。
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引用次数: 16
Creatine uptake regulates CD8 T cell antitumor immunity 肌酸摄取调节CD8 T细胞抗肿瘤免疫
Pub Date : 2019-10-18 DOI: 10.1084/jem.20182044
S. Di Biase, Xiaoya Ma, Xi Wang, Jiaji Yu, Yu-Chen Wang, Drake J. Smith, Yang Zhou, Zhe Li, Y. J. Kim, N. Clarke, Angela To, Lili Yang
Di Biase et al. show for the first time that creatine acts as a “molecular battery” conserving bioenergy to power CD8 T cell activities; that creatine uptake is critical in supporting antitumor T cell immunity; and that creatine supplementation holds promise for improving cancer immunotherapy.
Di Biase等人首次表明,肌酸作为一种“分子电池”,保存生物能量,为CD8 T细胞活动提供动力;肌酸摄取对支持抗肿瘤T细胞免疫至关重要;补充肌酸有望改善癌症免疫治疗。
{"title":"Creatine uptake regulates CD8 T cell antitumor immunity","authors":"S. Di Biase, Xiaoya Ma, Xi Wang, Jiaji Yu, Yu-Chen Wang, Drake J. Smith, Yang Zhou, Zhe Li, Y. J. Kim, N. Clarke, Angela To, Lili Yang","doi":"10.1084/jem.20182044","DOIUrl":"https://doi.org/10.1084/jem.20182044","url":null,"abstract":"Di Biase et al. show for the first time that creatine acts as a “molecular battery” conserving bioenergy to power CD8 T cell activities; that creatine uptake is critical in supporting antitumor T cell immunity; and that creatine supplementation holds promise for improving cancer immunotherapy.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90754139","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: 55
GM-CSF in inflammation 炎症中的GM-CSF
Pub Date : 2019-10-14 DOI: 10.1084/jem.20190945
J. Hamilton
GM-CSF is a potential therapeutic target in inflammation and autoimmunity. This study reviews the literature on the biology of GM-CSF, in particular that describing the research leading to clinical trials targeting GM-CSF and its receptor in numerous inflammatory/autoimmune conditions, such as rheumatoid arthritis.
GM-CSF是炎症和自身免疫的潜在治疗靶点。本研究回顾了有关GM-CSF生物学的文献,特别是描述了针对GM-CSF及其受体在许多炎症/自身免疫性疾病(如类风湿关节炎)中的临床试验的研究。
{"title":"GM-CSF in inflammation","authors":"J. Hamilton","doi":"10.1084/jem.20190945","DOIUrl":"https://doi.org/10.1084/jem.20190945","url":null,"abstract":"GM-CSF is a potential therapeutic target in inflammation and autoimmunity. This study reviews the literature on the biology of GM-CSF, in particular that describing the research leading to clinical trials targeting GM-CSF and its receptor in numerous inflammatory/autoimmune conditions, such as rheumatoid arthritis.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78590807","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: 152
Inflammasome signaling and regulation of interleukin-1 family cytokines 炎性小体的信号传导和白细胞介素-1家族细胞因子的调控
Pub Date : 2019-10-14 DOI: 10.1084/jem.20190314
A. Chan, K. Schroder
Specific IL-1 family cytokines are initially expressed as inactive, cytosolic pro-forms. Chan and Schroder review inflammasome signaling and cell death decisions, mechanisms underpinning IL-1α, IL-1β, IL-18, and IL-37 maturation and release, and the functions of these cytokines in protective and pathological inflammation.
特异性IL-1家族细胞因子最初以无活性的细胞质前形态表达。Chan和Schroder综述了炎症小体信号传导和细胞死亡决定,IL-1α、IL-1β、IL-18和IL-37成熟和释放的机制,以及这些细胞因子在保护性和病理性炎症中的功能。
{"title":"Inflammasome signaling and regulation of interleukin-1 family cytokines","authors":"A. Chan, K. Schroder","doi":"10.1084/jem.20190314","DOIUrl":"https://doi.org/10.1084/jem.20190314","url":null,"abstract":"Specific IL-1 family cytokines are initially expressed as inactive, cytosolic pro-forms. Chan and Schroder review inflammasome signaling and cell death decisions, mechanisms underpinning IL-1α, IL-1β, IL-18, and IL-37 maturation and release, and the functions of these cytokines in protective and pathological inflammation.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75935520","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: 204
Effects of interleukin-2 in immunostimulation and immunosuppression 白细胞介素-2在免疫刺激和免疫抑制中的作用
Pub Date : 2019-10-14 DOI: 10.1084/jem.20191247
Jonathan G. Pol, Pamela Caudana, J. Paillet, E. Piaggio, G. Kroemer
Distinctions in the nature and spatiotemporal expression of IL-2R subunits on conventional versus regulatory T cells are exploited to manipulate IL-2 immunomodulatory effects. Particularly, low-dose IL-2 and some recombinant derivatives are being evaluated to enhance/inhibit immune responses for therapeutic purposes.
IL-2R亚基在常规T细胞和调节性T细胞上的性质和时空表达的差异被用来操纵IL-2的免疫调节作用。特别是,正在评估低剂量IL-2和一些重组衍生物,以增强/抑制治疗目的的免疫反应。
{"title":"Effects of interleukin-2 in immunostimulation and immunosuppression","authors":"Jonathan G. Pol, Pamela Caudana, J. Paillet, E. Piaggio, G. Kroemer","doi":"10.1084/jem.20191247","DOIUrl":"https://doi.org/10.1084/jem.20191247","url":null,"abstract":"Distinctions in the nature and spatiotemporal expression of IL-2R subunits on conventional versus regulatory T cells are exploited to manipulate IL-2 immunomodulatory effects. Particularly, low-dose IL-2 and some recombinant derivatives are being evaluated to enhance/inhibit immune responses for therapeutic purposes.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84059956","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: 90
Biology and therapeutic potential of interleukin-10 白细胞介素-10的生物学和治疗潜力
Pub Date : 2019-10-14 DOI: 10.1084/jem.20190418
M. Saraiva, P. Vieira, A. O’Garra
The authors review the molecular mechanisms regulating IL-10 production and response and describe classic and novel functions of IL-10 in immune and non-immune cells. They further discuss the therapeutic potential of IL-10 in different diseases and the outstanding questions underlying an effective application of IL-10 in clinical settings.
本文综述了IL-10产生和应答的分子机制,并介绍了IL-10在免疫和非免疫细胞中的经典和新功能。他们进一步讨论了IL-10在不同疾病中的治疗潜力以及IL-10在临床环境中有效应用的潜在问题。
{"title":"Biology and therapeutic potential of interleukin-10","authors":"M. Saraiva, P. Vieira, A. O’Garra","doi":"10.1084/jem.20190418","DOIUrl":"https://doi.org/10.1084/jem.20190418","url":null,"abstract":"The authors review the molecular mechanisms regulating IL-10 production and response and describe classic and novel functions of IL-10 in immune and non-immune cells. They further discuss the therapeutic potential of IL-10 in different diseases and the outstanding questions underlying an effective application of IL-10 in clinical settings.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85909960","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: 367
Pathogenic T cell cytokines in multiple sclerosis 多发性硬化症中的致病性T细胞因子
Pub Date : 2019-10-14 DOI: 10.1084/jem.20190460
Catriona A Wagner, Pamela J. Roqué, J. Goverman
This review summarizes our current understanding of how specific cytokines produced by pathogenic CD4 T cells contribute to central nervous system autoimmune disease. Data obtained from animal models and patients with multiple sclerosis are discussed.
这篇综述总结了我们目前对致病性CD4 T细胞产生的特异性细胞因子如何促进中枢神经系统自身免疫性疾病的理解。从动物模型和多发性硬化症患者中获得的数据进行了讨论。
{"title":"Pathogenic T cell cytokines in multiple sclerosis","authors":"Catriona A Wagner, Pamela J. Roqué, J. Goverman","doi":"10.1084/jem.20190460","DOIUrl":"https://doi.org/10.1084/jem.20190460","url":null,"abstract":"This review summarizes our current understanding of how specific cytokines produced by pathogenic CD4 T cells contribute to central nervous system autoimmune disease. Data obtained from animal models and patients with multiple sclerosis are discussed.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77265513","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
A homozygous SFTPA1 mutation drives necroptosis of type II alveolar epithelial cells in patients with idiopathic pulmonary fibrosis 纯合子SFTPA1突变驱动特发性肺纤维化患者II型肺泡上皮细胞坏死
Pub Date : 2019-10-10 DOI: 10.1084/jem.20182351
Akio Takezaki, S. Tsukumo, Y. Setoguchi, J. Ledford, H. Goto, K. Hosomichi, H. Uehara, Y. Nishioka, K. Yasutomo
We identify a homozygous mutation in SFTPA1 in patients with idiopathic pulmonary fibrosis (IPF). The mutation causes increased necroptosis of type II alveolar epithelial cells through the IRE1α–JNK axis, which highlights the necroptosis pathway as a therapeutic target for IPF.
我们在特发性肺纤维化(IPF)患者中发现了SFTPA1的纯合突变。该突变通过IRE1α-JNK轴导致II型肺泡上皮细胞坏死性凋亡增加,这突出了坏死性凋亡途径作为IPF的治疗靶点。
{"title":"A homozygous SFTPA1 mutation drives necroptosis of type II alveolar epithelial cells in patients with idiopathic pulmonary fibrosis","authors":"Akio Takezaki, S. Tsukumo, Y. Setoguchi, J. Ledford, H. Goto, K. Hosomichi, H. Uehara, Y. Nishioka, K. Yasutomo","doi":"10.1084/jem.20182351","DOIUrl":"https://doi.org/10.1084/jem.20182351","url":null,"abstract":"We identify a homozygous mutation in SFTPA1 in patients with idiopathic pulmonary fibrosis (IPF). The mutation causes increased necroptosis of type II alveolar epithelial cells through the IRE1α–JNK axis, which highlights the necroptosis pathway as a therapeutic target for IPF.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80602377","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: 45
Modulation of the fungal mycobiome is regulated by the chitin-binding receptor FIBCD1 真菌菌群的调节是由几丁质结合受体FIBCD1调控的
Pub Date : 2019-10-10 DOI: 10.1084/jem.20182244
J. B. Moeller, Irina Leonardi, A. Schlosser, A. Flamar, N. Bessman, G. Putzel, T. Thomsen, Mark A. Hammond, C. S. Jepsen, K. Skjødt, E. Füchtbauer, D. Farber, G. Sørensen, I. Iliev, U. Holmskov, D. Artis
In the present study, Moeller et al. identify a previously unrecognized pathway through which intestinal epithelial cells expressing the novel chitin-binding receptor FIBCD1 can recognize and control intestinal fungal colonization, limit fungal dysbiosis, and dampen intestinal inflammation.
在本研究中,Moeller等人发现了一种以前未被识别的途径,通过该途径,表达新型几丁质结合受体ficd1的肠上皮细胞可以识别和控制肠道真菌定植,限制真菌生态失调,并抑制肠道炎症。
{"title":"Modulation of the fungal mycobiome is regulated by the chitin-binding receptor FIBCD1","authors":"J. B. Moeller, Irina Leonardi, A. Schlosser, A. Flamar, N. Bessman, G. Putzel, T. Thomsen, Mark A. Hammond, C. S. Jepsen, K. Skjødt, E. Füchtbauer, D. Farber, G. Sørensen, I. Iliev, U. Holmskov, D. Artis","doi":"10.1084/jem.20182244","DOIUrl":"https://doi.org/10.1084/jem.20182244","url":null,"abstract":"In the present study, Moeller et al. identify a previously unrecognized pathway through which intestinal epithelial cells expressing the novel chitin-binding receptor FIBCD1 can recognize and control intestinal fungal colonization, limit fungal dysbiosis, and dampen intestinal inflammation.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90540898","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: 19
Microglia drive APOE-dependent neurodegeneration in a tauopathy mouse model 小胶质细胞驱动apoe依赖性脑损伤小鼠模型的神经变性
Pub Date : 2019-10-10 DOI: 10.1084/jem.20190980
Yang Shi, Melissa Manis, J. Long, Kairuo Wang, P. Sullivan, Javier Remolina Serrano, Rosa Hoyle, D. Holtzman
Shi et al. find that microglia, instead of tau-induced direct neurotoxicity, are the driving force of neurodegeneration in a tauopathy mouse model. Microglia are also required for tau pathogenesis. In addition, apoE strongly regulates neurodegeneration in the setting of tauopathy predominantly by modulating microglial function.
Shi等人发现,在牛头病小鼠模型中,小胶质细胞而不是tau诱导的直接神经毒性是神经退行性变的驱动力。小胶质细胞也是tau发病所必需的。此外,apoE主要通过调节小胶质细胞功能,在牛头病的情况下强烈调节神经退行性变。
{"title":"Microglia drive APOE-dependent neurodegeneration in a tauopathy mouse model","authors":"Yang Shi, Melissa Manis, J. Long, Kairuo Wang, P. Sullivan, Javier Remolina Serrano, Rosa Hoyle, D. Holtzman","doi":"10.1084/jem.20190980","DOIUrl":"https://doi.org/10.1084/jem.20190980","url":null,"abstract":"Shi et al. find that microglia, instead of tau-induced direct neurotoxicity, are the driving force of neurodegeneration in a tauopathy mouse model. Microglia are also required for tau pathogenesis. In addition, apoE strongly regulates neurodegeneration in the setting of tauopathy predominantly by modulating microglial function.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89900988","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: 218
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The Tokushima journal of experimental medicine
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