My Mentor Howard A. Young.
作者信息
Hoshino Tomoaki
机构信息
NCI-Frederick, Fredrick, Maryland, USA.
Chest Disease Center, Kurume University Hospital, Kurume, Fukuoka, Japan.
出版信息
J Interferon Cytokine Res. 2022 Dec;42(12):605-607. doi: 10.1089/jir.2022.0074. Epub 2022 Jun 8.
Abstract
摘要
相似文献
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本文引用的文献
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Interleukin-18 in pulmonary inflammatory diseases.白细胞介素-18 在肺部炎症性疾病中的作用。
J Interferon Cytokine Res. 2012 Oct;32(10):443-9. doi: 10.1089/jir.2012.0029. Epub 2012 Aug 17.
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Role of proinflammatory cytokines IL-18 and IL-1beta in bleomycin-induced lung injury in humans and mice.促炎细胞因子IL-18和IL-1β在博来霉素诱导的人和小鼠肺损伤中的作用。
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Cytokines in pulmonary emphysema: can results in mice be translated to humans?肺气肿中的细胞因子：小鼠实验结果能否应用于人类？
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Pulmonary inflammation and emphysema: role of the cytokines IL-18 and IL-13.肺部炎症与肺气肿：细胞因子白细胞介素-18和白细胞介素-13的作用
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5
Thioredoxin suppresses airway hyperresponsiveness and airway inflammation in asthma.硫氧还蛋白可抑制哮喘中的气道高反应性和气道炎症。
Biochem Biophys Res Commun. 2005 Sep 9;334(4):1141-8. doi: 10.1016/j.bbrc.2005.07.007.
6
Redox-active protein thioredoxin prevents proinflammatory cytokine- or bleomycin-induced lung injury.氧化还原活性蛋白硫氧还蛋白可预防促炎细胞因子或博来霉素诱导的肺损伤。
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7
Interleukin 18 (IL-18) in synergy with IL-2 induces lethal lung injury in mice: a potential role for cytokines, chemokines, and natural killer cells in the pathogenesis of interstitial pneumonia.白细胞介素18（IL-18）与IL-2协同作用可诱导小鼠发生致死性肺损伤：细胞因子、趋化因子和自然杀伤细胞在间质性肺炎发病机制中的潜在作用
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8
Cutting edge: IL-18-transgenic mice: in vivo evidence of a broad role for IL-18 in modulating immune function.前沿：白细胞介素-18转基因小鼠：白细胞介素-18在调节免疫功能中广泛作用的体内证据。
J Immunol. 2001 Jun 15;166(12):7014-8. doi: 10.4049/jimmunol.166.12.7014.
9
Functional reconstitution and regulation of IL-18 activity by the IL-18R beta chain.IL-18Rβ链对IL-18活性的功能重建与调节
J Immunol. 2001 Jan 1;166(1):148-54. doi: 10.4049/jimmunol.166.1.148.
10
In vivo administration of IL-18 can induce IgE production through Th2 cytokine induction and up-regulation of CD40 ligand (CD154) expression on CD4+ T cells.体内给予白细胞介素-18可通过诱导Th2细胞因子和上调CD4⁺T细胞上的CD40配体（CD154）表达来诱导IgE产生。
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