Eleanor A Fallon相关文献与解析，生知库 | 链接生命科学的每一步

Anne-Lise Rossi, Marilyn Le, Chun-Shiang Chung, Yaping Chen, Eleanor A Fallon, Andres Matoso, Shumin Xu, Tristen T Chun, Craig P Erickson, Alfred Ayala

细胞生物学

其它细胞

发表日期：2019

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Herpes Virus Entry Mediator (HVEM) Expression Promotes Inflammation/ Organ Injury in Response to Experimental Indirect-Acute Lung Injury

疱疹病毒进入介质 (HVEM) 表达促进实验性间接急性肺损伤引起的炎症/器官损伤

期刊:Shock

影响因子:2.7

doi:10.1097/SHK.0000000000001174

Tingting Cheng, Jianwen Bai, Chun-Shiang Chung, Yaping Chen, Eleanor A Fallon, Alfred Ayala

免疫

微生物学

疱疹

Immunology/Inflammation

发表日期：2019

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Group 2 Innate Lymphoid Cells (ILC2s) Are Key Mediators of the Inflammatory Response in Polymicrobial Sepsis

第 2 组先天淋巴细胞 (ILC2) 是多重微生物脓毒症炎症反应的关键介质

期刊:American Journal of Pathology

影响因子:4.7

doi:10.1016/j.ajpath.2018.05.009

Tristen T Chun, Chun-Shiang Chung, Eleanor A Fallon, Noelle A Hutchins, Erlyana Clarke, Anne-Lise Rossi, William G Cioffi, Daithi S Heffernan, Alfred Ayala

PAD4 Deficiency Leads to Decreased Organ Dysfunction and Improved Survival in a Dual Insult Model of Hemorrhagic Shock and Sepsis

PAD4 缺乏可减少失血性休克和脓毒症双重损伤模型中的器官功能障碍并提高生存率

期刊:Journal of Immunology

影响因子:3.6

doi:10.4049/jimmunol.1700639

Bethany M Biron, Chun-Shiang Chung, Yaping Chen, Zachary Wilson, Eleanor A Fallon, Jonathan S Reichner, Alfred Ayala

信号转导

发表日期：2018

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Program Cell Death Receptor-1-Mediated Invariant Natural Killer T-Cell Control of Peritoneal Macrophage Modulates Survival in Neonatal Sepsis

程序性细胞死亡受体-1 介导的恒定自然杀伤 T 细胞控制腹膜巨噬细胞调节新生儿脓毒症的生存率

期刊:Frontiers in Immunology

影响因子:5.7

doi:10.3389/fimmu.2017.01469

Eleanor A Fallon, Tristen T Chun, Whitney A Young, Chyna Gray, Alfred Ayala, Daithi S Heffernan

A novel role for programmed cell death receptor ligand 2 in sepsis-induced hepatic dysfunction

程序性细胞死亡受体配体 2 在脓毒症引起的肝功能障碍中的新作用

Herpes Virus Entry Mediator (HVEM) Expression Promotes Inflammation/ Organ Injury in Response to Experimental Indirect-Acute Lung Injury

疱疹病毒进入介质 (HVEM) 表达促进实验性间接急性肺损伤引起的炎症/器官损伤

Group 2 Innate Lymphoid Cells (ILC2s) Are Key Mediators of the Inflammatory Response in Polymicrobial Sepsis

第 2 组先天淋巴细胞 (ILC2) 是多重微生物脓毒症炎症反应的关键介质

PAD4 Deficiency Leads to Decreased Organ Dysfunction and Improved Survival in a Dual Insult Model of Hemorrhagic Shock and Sepsis

PAD4 缺乏可减少失血性休克和脓毒症双重损伤模型中的器官功能障碍并提高生存率

Program Cell Death Receptor-1-Mediated Invariant Natural Killer T-Cell Control of Peritoneal Macrophage Modulates Survival in Neonatal Sepsis

程序性细胞死亡受体-1 介导的恒定自然杀伤 T 细胞控制腹膜巨噬细胞调节新生儿脓毒症的生存率