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The Tokushima journal of experimental medicine最新文献

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Concomitant PIK3CD and TNFRSF9 deficiencies cause chronic active Epstein-Barr virus infection of T cells 伴随的PIK3CD和TNFRSF9缺陷导致T细胞的慢性活动性eb病毒感染
Pub Date : 2019-09-19 DOI: 10.1084/jem.20190678
Rémy Rodriguez, B. Fournier, D. J. Cordeiro, Sarah Winter, K. Izawa, Emmanuel Martin, D. Boutboul, C. Lenoir, S. Fraitag, S. Kracker, T. Watts, C. Picard, J. Bruneau, I. Callebaut, A. Fischer, B. Neven, S. Latour
Identification of biallelic loss-of-function mutations in TNFRSF9 and PIK3CD in a kindred with chronic active Epstein-Barr virus infection of T cells (CAEBV) suggests that CAEBV is the consequence of factors providing growth advantage to EBV-infected T cells combined with defective cell immunity toward EBV-infected cells.
在慢性活动性eb病毒感染T细胞(CAEBV)的亲属中鉴定出TNFRSF9和PIK3CD双等位基因功能缺失突变,表明CAEBV是提供ebv感染T细胞生长优势的因素结合对ebv感染细胞的缺陷细胞免疫的结果。
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引用次数: 50
TGF-β signaling controls Foxp3 methylation and T reg cell differentiation by modulating Uhrf1 activity TGF-β信号通过调节Uhrf1活性控制Foxp3甲基化和T细胞分化
Pub Date : 2019-09-12 DOI: 10.1084/jem.20190550
Xiang Sun, Yu Cui, Haiyun Feng, Haifeng Liu, Xiaolong Liu
How DNA methylation–mediated repression is reversed before Foxp3 transcription is unclear. Here, Sun et al. show that the epigenetic regulator Uhrf1, which maintained Foxp3 methylation, is down-regulated by TGF-β signaling and provide novel insight into the epigenetic regulation of Foxp3 during iT reg cell differentiation.
在Foxp3转录之前,DNA甲基化介导的抑制是如何被逆转的尚不清楚。在这里,Sun等人发现维持Foxp3甲基化的表观遗传调控因子Uhrf1被TGF-β信号下调,并为iT regg细胞分化过程中Foxp3的表观遗传调控提供了新的见解。
{"title":"TGF-β signaling controls Foxp3 methylation and T reg cell differentiation by modulating Uhrf1 activity","authors":"Xiang Sun, Yu Cui, Haiyun Feng, Haifeng Liu, Xiaolong Liu","doi":"10.1084/jem.20190550","DOIUrl":"https://doi.org/10.1084/jem.20190550","url":null,"abstract":"How DNA methylation–mediated repression is reversed before Foxp3 transcription is unclear. Here, Sun et al. show that the epigenetic regulator Uhrf1, which maintained Foxp3 methylation, is down-regulated by TGF-β signaling and provide novel insight into the epigenetic regulation of Foxp3 during iT reg cell differentiation.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":"29 1","pages":"2819 - 2837"},"PeriodicalIF":0.0,"publicationDate":"2019-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77790057","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: 42
Tumors with TSC mutations are sensitive to CDK7 inhibition through NRF2 and glutathione depletion TSC突变的肿瘤通过NRF2和谷胱甘肽耗竭对CDK7抑制敏感
Pub Date : 2019-09-10 DOI: 10.1084/jem.20190251
Mahsa Zarei, H. Du, A. Nassar, Rachel E Yan, K. Giannikou, Sneha Johnson, H. Lam, E. Henske, Yubao Wang, Tinghu Zhang, J. Asara, D. Kwiatkowski
Tuberous sclerosis complex (TSC) is a genetic disorder in which tumors develop due to TSC1/TSC2 loss and activation of mTORC1. Zarei et al. show that TSC tumors are sensitive to CDK7 inhibition, which reduces expression of NRF2 and glutathione synthetic genes, leading to glutathione depletion and ROS-mediated cell death.
结节性硬化症(TSC)是一种由于TSC1/TSC2缺失和mTORC1激活而导致肿瘤发展的遗传性疾病。Zarei等研究表明,TSC肿瘤对CDK7抑制敏感,CDK7抑制可降低NRF2和谷胱甘肽合成基因的表达,导致谷胱甘肽耗损和ros介导的细胞死亡。
{"title":"Tumors with TSC mutations are sensitive to CDK7 inhibition through NRF2 and glutathione depletion","authors":"Mahsa Zarei, H. Du, A. Nassar, Rachel E Yan, K. Giannikou, Sneha Johnson, H. Lam, E. Henske, Yubao Wang, Tinghu Zhang, J. Asara, D. Kwiatkowski","doi":"10.1084/jem.20190251","DOIUrl":"https://doi.org/10.1084/jem.20190251","url":null,"abstract":"Tuberous sclerosis complex (TSC) is a genetic disorder in which tumors develop due to TSC1/TSC2 loss and activation of mTORC1. Zarei et al. show that TSC tumors are sensitive to CDK7 inhibition, which reduces expression of NRF2 and glutathione synthetic genes, leading to glutathione depletion and ROS-mediated cell death.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":"216 1","pages":"2635 - 2652"},"PeriodicalIF":0.0,"publicationDate":"2019-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75371534","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: 15
TGFβ signaling in germinal center B cells promotes the transition from light zone to dark zone 生发中心B细胞中的tgf - β信号传导促进了从亮区到暗区的转变
Pub Date : 2019-09-10 DOI: 10.1084/jem.20181868
Anne R Albright, J. Kabat, Moyi Li, Fiona Raso, A. Reboldi, J. Muppidi
GCs are polarized into LZ and DZ to allow for the spatial separation of selection and proliferation. In this study, we describe the previously unknown function of TGFβ in promoting the transition of GCBs from LZ to DZ.
GCs被极化为LZ和DZ,以允许选择和增殖的空间分离。在这项研究中,我们描述了TGFβ在促进gcb从LZ向DZ转变中的先前未知的功能。
{"title":"TGFβ signaling in germinal center B cells promotes the transition from light zone to dark zone","authors":"Anne R Albright, J. Kabat, Moyi Li, Fiona Raso, A. Reboldi, J. Muppidi","doi":"10.1084/jem.20181868","DOIUrl":"https://doi.org/10.1084/jem.20181868","url":null,"abstract":"GCs are polarized into LZ and DZ to allow for the spatial separation of selection and proliferation. In this study, we describe the previously unknown function of TGFβ in promoting the transition of GCBs from LZ to DZ.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":"238 1 1","pages":"2531 - 2545"},"PeriodicalIF":0.0,"publicationDate":"2019-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72948921","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: 18
Cytosolic PCNA interacts with p47phox and controls NADPH oxidase NOX2 activation in neutrophils 细胞质内PCNA与p47phox相互作用并控制中性粒细胞中NADPH氧化酶NOX2的激活
Pub Date : 2019-09-06 DOI: 10.1084/jem.20180371
Delphine Ohayon, Alessia De Chiara, P. M. Dang, N. Thieblemont, Simon M. Chatfield, V. Marzaioli, S. S. Burgener, Julie Mocek, C. Candalh, Coralie Pintard, P. Tacnet-Delorme, G. Renault, I. Lagoutte, M. Favier, Francine Walker, M. Hurtado-Nedelec, D. Desplancq, E. Weiss, C. Benarafa, D. Housset, J. Marie, P. Frachet, J. El-Benna, V. Witko-Sarsat
This study describes a novel function of cytosolic proliferating cell nuclear antigen (PCNA) in the control of neutrophil NADPH oxidase, a complex pivotal for ROS generation in inflammation. Inhibition of neutrophil PCNA results in a potent antiinflammatory effect in colitis.
本研究描述了胞质增殖细胞核抗原(PCNA)在控制中性粒细胞NADPH氧化酶中的新功能,而中性粒细胞NADPH氧化酶是炎症中ROS生成的关键复合物。抑制中性粒细胞PCNA在结肠炎中具有有效的抗炎作用。
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引用次数: 22
An anti-CRF antibody suppresses the HPA axis and reverses stress-induced phenotypes 抗crf抗体抑制HPA轴并逆转应激诱导的表型
Pub Date : 2019-08-29 DOI: 10.1084/jem.20190430
Hunter S. Futch, Karen N. McFarland, Brenda D. Moore, M. Zino Kuhn, B. Giasson, Thomas B. Ladd, Karen A. Scott, Melanie R. Shapiro, Rachel L. Nosacka, Marshall S. Goodwin, Yong Ran, Pedro E. Cruz, Daniel H. Ryu, Cara L. Croft, Yona Levites, C. Janus, Paramita Chakrabarty, Andrew R. Judge, T. Brusko, A. D. de Kloet, E. Krause, T. Golde
A high-affinity monoclonal antibody (CTRND05) targeting corticotropin-releasing factor (CRF) blocks stress-induced corticosterone increases, counteracts effects of chronic variable stress, and induces other phenotypes consistent with suppression of the HPA axis.
一种靶向促肾上腺皮质激素释放因子(CRF)的高亲和力单克隆抗体(CTRND05)可阻断应激诱导的皮质酮增加,抵消慢性可变应激的影响,并诱导与HPA轴抑制一致的其他表型。
{"title":"An anti-CRF antibody suppresses the HPA axis and reverses stress-induced phenotypes","authors":"Hunter S. Futch, Karen N. McFarland, Brenda D. Moore, M. Zino Kuhn, B. Giasson, Thomas B. Ladd, Karen A. Scott, Melanie R. Shapiro, Rachel L. Nosacka, Marshall S. Goodwin, Yong Ran, Pedro E. Cruz, Daniel H. Ryu, Cara L. Croft, Yona Levites, C. Janus, Paramita Chakrabarty, Andrew R. Judge, T. Brusko, A. D. de Kloet, E. Krause, T. Golde","doi":"10.1084/jem.20190430","DOIUrl":"https://doi.org/10.1084/jem.20190430","url":null,"abstract":"A high-affinity monoclonal antibody (CTRND05) targeting corticotropin-releasing factor (CRF) blocks stress-induced corticosterone increases, counteracts effects of chronic variable stress, and induces other phenotypes consistent with suppression of the HPA axis.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":"43 1","pages":"2479 - 2491"},"PeriodicalIF":0.0,"publicationDate":"2019-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78956950","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
Gasdermin D in peripheral myeloid cells drives neuroinflammation in experimental autoimmune encephalomyelitis 实验性自身免疫性脑脊髓炎中外周髓细胞的气真皮蛋白D驱动神经炎症
Pub Date : 2019-08-29 DOI: 10.1084/jem.20190377
Sheng Li, Yuqing Wu, Dongxue Yang, Chunyan Wu, Chunmei Ma, Xue Liu, P. Moynagh, Bingwei Wang, G. Hu, Shuo Yang
In this study, Li et al. demonstrate that gasdermin D in peripheral myeloid cells promotes the activation and differentiation of T cell in the secondary lymphoid organs, thus driving T cell–mediated neuroinflammation and demyelination in the CNS of EAE mice.
Li等在本研究中发现,外周髓细胞中的gasdermin D可促进次级淋巴器官中T细胞的活化和分化,从而驱动EAE小鼠中枢神经系统中T细胞介导的神经炎症和脱髓鞘。
{"title":"Gasdermin D in peripheral myeloid cells drives neuroinflammation in experimental autoimmune encephalomyelitis","authors":"Sheng Li, Yuqing Wu, Dongxue Yang, Chunyan Wu, Chunmei Ma, Xue Liu, P. Moynagh, Bingwei Wang, G. Hu, Shuo Yang","doi":"10.1084/jem.20190377","DOIUrl":"https://doi.org/10.1084/jem.20190377","url":null,"abstract":"In this study, Li et al. demonstrate that gasdermin D in peripheral myeloid cells promotes the activation and differentiation of T cell in the secondary lymphoid organs, thus driving T cell–mediated neuroinflammation and demyelination in the CNS of EAE mice.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":"119 1","pages":"2562 - 2581"},"PeriodicalIF":0.0,"publicationDate":"2019-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85635338","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: 111
Correction: Heterotypic CAF-tumor spheroids promote early peritoneal metastatis of ovarian cancer 更正:异型caf -肿瘤球体促进卵巢癌早期腹膜转移
Pub Date : 2019-08-26 DOI: 10.1084/jem.2018076508222019C
Qing-cui Gao, Zong-Yuan Yang, Sen Xu, Xiaoting Li, Xin Yang, P. Jin, Yi Liu, Xiaoshui Zhou, Taoran Zhang, Cheng Gong, Xiao Wei, Dan Liu, Chaoyang Sun, Gang Chen, Junbo Hu, L. Meng, Jianfeng Zhou, Kenjiro Sawada, R. Fruscio, T. Grunt, J. Wischhusen, V. Vargas-Hernández, B. Pothuri, R. Coleman
2448 https://doi.org/10.1084/jem.20180765 J. Exp. Med. 2019 Vol. 216 No. 1
2448 https://doi.org/10.1084/jem.20180765中华检验医学杂志,2019 Vol. 216 No. 1
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引用次数: 4
Ross Levine: Focus on the critical questions Ross Levine:关注关键问题
Pub Date : 2019-08-22 DOI: 10.1084/jem.20191484
S. Houston
Ross Levine: Focus on the critical questions
Ross Levine:关注关键问题
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引用次数: 0
Yeats4 drives ILC lineage commitment via activation of Lmo4 transcription Yeats4通过激活Lmo4转录驱动ILC谱系承诺
Pub Date : 2019-08-21 DOI: 10.1084/jem.20182363
Benyu Liu, Liuliu Yang, Xiaoxiao Zhu, Huimu Li, P. Zhu, Jiayi Wu, Tiankun Lu, Luyun He, Nian Liu, Shu Meng, Liang Zhou, B. Ye, Yong Tian, Z. Fan
Liu et al. show that Yeats4 recruits the Dot1l–RNA Pol II complex onto the Lmo4 promoter by recognizing H3K27ac modification to initiate Lmo4 transcription in α4β7+ CLPs, leading to ILC lineage commitment.
Liu等人的研究表明,yeat4通过识别H3K27ac修饰,将Dot1l-RNA Pol II复合物招募到Lmo4启动子上,启动α4β7+ CLPs中的Lmo4转录,从而导致ILC谱系承诺。
{"title":"Yeats4 drives ILC lineage commitment via activation of Lmo4 transcription","authors":"Benyu Liu, Liuliu Yang, Xiaoxiao Zhu, Huimu Li, P. Zhu, Jiayi Wu, Tiankun Lu, Luyun He, Nian Liu, Shu Meng, Liang Zhou, B. Ye, Yong Tian, Z. Fan","doi":"10.1084/jem.20182363","DOIUrl":"https://doi.org/10.1084/jem.20182363","url":null,"abstract":"Liu et al. show that Yeats4 recruits the Dot1l–RNA Pol II complex onto the Lmo4 promoter by recognizing H3K27ac modification to initiate Lmo4 transcription in α4β7+ CLPs, leading to ILC lineage commitment.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":"64 1","pages":"2653 - 2668"},"PeriodicalIF":0.0,"publicationDate":"2019-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83309123","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: 11
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The Tokushima journal of experimental medicine
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