Is TLR4 Critical for Neutrophil Apoptosis in Occupational Asthma?
作者信息
Choi Youngwoo, Sim Soyoon, Park Hae Sim
机构信息
Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
出版信息
Allergy Asthma Immunol Res. 2020 Jul;12(4):560-562. doi: 10.4168/aair.2020.12.4.560.
Abstract
摘要
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Is TLR4 Critical for Neutrophil Apoptosis in Occupational Asthma?Toll样受体4在职业性哮喘中性粒细胞凋亡中起关键作用吗？
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本文引用的文献
1
Toll-like Receptor 4 Deficiency Aggravates Airway Hyperresponsiveness and Inflammation by Impairing Neutrophil Apoptosis in a Toluene Diisocyanate-Induced Murine Asthma Model.在甲苯二异氰酸酯诱导的小鼠哮喘模型中，Toll样受体4缺陷通过损害中性粒细胞凋亡加重气道高反应性和炎症。
Allergy Asthma Immunol Res. 2020 Jul;12(4):608-625. doi: 10.4168/aair.2020.12.4.608.
2
Adeno-associated Virus 9-mediated Small RNA Interference of TLR4 Alleviates Myocardial Ischemia and Reperfusion Injury by Inhibition of the NF-κB and MAPK Signaling Pathways in Rats.腺相关病毒 9 介导的 TLR4 小干扰 RNA 通过抑制 NF-κB 和 MAPK 信号通路减轻大鼠心肌缺血再灌注损伤。
Curr Mol Med. 2019;19(2):127-135. doi: 10.2174/1566524019666190311122521.
3
Update on the Management of Occupational Asthma and Work-Exacerbated Asthma.职业性哮喘和工作性加重哮喘管理的最新进展
Allergy Asthma Immunol Res. 2019 Mar;11(2):188-200. doi: 10.4168/aair.2019.11.2.188.
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Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins.凋亡在健康和疾病中的调控：BCL-2 家族蛋白的平衡作用。
Nat Rev Mol Cell Biol. 2019 Mar;20(3):175-193. doi: 10.1038/s41580-018-0089-8.
5
IL-17F, rather than IL-17A, underlies airway inflammation in a steroid-insensitive toluene diisocyanate-induced asthma model.白细胞介素-17F（IL-17F）而非白细胞介素-17A（IL-17A）是甲苯二异氰酸酯（TDI）诱导的哮喘模型中类固醇不敏感气道炎症的基础。
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Occupational asthma risk from exposures to toluene diisocyanate: A review and risk assessment.甲苯二异氰酸酯所致职业性哮喘的风险：综述与风险评估。
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Front Physiol. 2017 Jul 19;8:508. doi: 10.3389/fphys.2017.00508. eCollection 2017.
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Cells and mediators in diisocyanate-induced occupational asthma.二异氰酸酯所致职业性哮喘的细胞和介质。
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The role of Toll-like receptors in the regulation of neutrophil migration, activation, and apoptosis.Toll样受体在调节中性粒细胞迁移、活化和凋亡中的作用。
Clin Infect Dis. 2005 Nov 15;41 Suppl 7:S421-6. doi: 10.1086/431992.
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